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Old 01-06-2005, 01:00 AM   #26
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Originally Posted by SuperSport
Sorry it took a while for me to get here Sweaty et al. Interesting thread.....

I believe Kevin is right in some of the info you posted Sweat. As for the shower being a gas chamber...well he has a point. Alot of our municipal water supplies are treated with fluoride (as is toothpaste) . Fluoride is a known poison of the highest degree. Fluoride was first introduced into the public water systems in the US in 1945 in an experiment that grew out of research done by H. Trendley Dean,DDS aka *the Father of Fluoridation*. for the Public Health Services. Dr. Dean was trying to determine why some people had staining on their teeth-his finding stated it was from fluoride, but he also credited fluoride as the reason these people with stained teeth had fewer cavities.
In 1950 the Public Health System recommended adding fluoride to water systems to fight tooth decay. However, even with the addition of fluoride to the water supplies cavity rates did not go down.
And.....the good Dr. has admitted on at least 2 occasions in the court of law that his original statistics favoring fluoridation were invalid. Kopf,C. "Doctor Who Advocated Fluoridation Now Calls It A Fraud" The Forum Health Freedom News 11 no6 (jul/aug 1992): 28.

We also absorb fluoride when taking a shower...and fluoride is classified as *very toxic to extremely toxic* by the National Library of Medicine. It is a well known carcinogen of the highest order. The reason the ADA and other agencies will not ban fluoride is because (IMO) it would set off a slew of class action lawsuits. Fluoride has been banned by many European countries . And fluoride also deposits aluminum in our brains....that leads to Alzheimer's.

Our food supply is absolute garbage. Take a look at the Health Forum here at IM and check out the Food Dangers and Factors of Disease. The FDA has approved no fewer than 400 chemicals that can be sprayed on crops. The latest craze is Genetically Modified (aka Genetically Engineered) foods. These foods are also much so that Europe has either banned most of them or all of them. These GM foods are designed to only increase yield...never to improve quality. I am in a field closely related to agriculture...and I know for a fact (at least several years ago) that lending institutions WILL NOT lend money to a farmer that does not spray chemicals on the crops. Everyone only cares about yield.
I am hoping some of this will change with the increased demand for organic foods.

As for the Rx companies.....yes, they only care about their bottom line. All we have to do is look at the Baycol debacle (100 plus people killed), Vioxx, Celebrex, et al....

I can (and will) cite several instances of non compliance with mandatory FDA trials and misrepresentation in advertising later in this thread. I will come back to it....I am just itching to get to the post that xRAJAx put up,lol.


I am very sure you put up that copy and paste without realizing who and what *Quackwatch* is. I am hoping you don't take this personally, 'cause it ain't meant that way. If you knew who is behind quackwatch I seriously doubt you would post anything from there.

Quackwatch is a website/business/scam run by none other than Stephen Barrett. Mr. Barrett likes to call himself *Dr. Barrett,MD*...but that is a lie. Fact of the matter is he had to surrender his medical liscense in the early mid nineties. He was a shrink. to all the medications this turd has taken he has rendered himself impotent (he admitted this in court). It couldn't happen to a nicer guy. Frankly, I am glad he can not spread his ignorance by not being able to procreate.

Since Mr Barrett lost his medical liscense he has had to forge out a living by trying to take alternative MD's to court for civil litigation and processes. He is (IMO) supported by big pharma.

This is what Barrett did early on before people got wise to him. He would take an MD to court over something trivial and offer the MD a settlement out of court. This is a great option for an MD or business-because if you don't go to court you do not have the possibility of losing-and you can seal the record so it is not made public. It is very possible that *Kevin* used this option himself.

Guess who has used this option before? Big pharma. And guess what for? HIV antibody tests. Yep...these *tests* are absolute garbage...and the smart people that have tested *positive* have taken the test kit manufacturer to court over the flaws in this testing. But no one really hears about it b/c the Pharma Co. always settles out of court. They are being taken to court now by Kim Bannon of Kansas. And the Pharma co has tried to settle with her-but she has told them to stick their millions where the sun don't shine-she wants their asses in court.
Ah..but I digress. xRAJAx knows how much I enjoy poking the HIV/AIDS establishment...

Let me get back to this Barrett fellow.

So...Barrett used to get lots of settlements this way. But finally some practitioners called his bluff....and went to court agaianst him. Barrett's court record is horrible-actually I don't think he has ever won a case. The biggest one he was involved in was about 2 years ago with Dr. Hulda Clark. Clark has a cancer clinic in Mexico with a very large following. She uses *frequency medicine*-the use of electrical current to kill cancer and viruses pretty good too. She also has alot of naturopathic flushes and such...I used her Gall Bladder flush-I got hundreds of gall stones out. It cost all of 6 bucks or so versus the 10K for gall bladder surgery. And I still have my gall bladder.I wonder why conventional medicine doesn't embrace such methods?

Anyway..back to Barrett. So anyway...Barrett tried to scam Dr. Clark is what it boiled down to. Totally blew up in his face. He was ordered by the court to *cease and desist*

The court also ridiculed him for his novel idea that Dr. Clark shouldn't be on the internet or some crazy idea like that.....

One of these days I will make a thread just for Barrett. He is a punk. And he still calls himself *Dr*.......lmao. Guess not being able to get it up does weird things to a guy...


Glad you responded to this thread. As for Quackwatch....I did not post that knowing who they are, and you point out some interesting points. But regardless of them, I do believe that the article is from the FTC, and can be found in its archive. Quackwatch seems to have added it to their site. If I'm mistaken, I apoligize.

The article was my focus...not quackwatch....and I do appreciate the info my friend. I just have an issue with snake oil informercials that have a cure for Kevin pretty much had his hand on every health indication via all his programs. Do you believe that his methods to raise your IQ and keep your blood pH at a healthy level to be benificial to us? These are just two examples of many. This is were I disagree if you believe his statements. As for everything else, I agree with your points. I still wouldn't touch his products without proven tests.

Now as for the HIV antibody test If you do recall our last discussion I spoke of NAT or Nucleic Acid testing which tests the virus at the RNA level. It is what test ALL of the US blood supply. It can isolate the virus. Hell I've replicated the Gag Pol and Gag Env of the virus myself at work for use in our vaccine. If you like I can send you the articles as the process was created by a scientist named Derek O'hegan and Manmohan Singh. Both were my mentors at work, and the process is patented and published in various peer reviewd journals. So as to whether it exists I think we've wasted enough of Winnie's Bandwith from our last discussion. I'll just have to agree to disagree with you. I do however enjoy your insight as it is very insightful. Maybe someday in our travels we'll be able to cross paths and exchange ideas....I would enjoy the exchange.


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Old 01-06-2005, 01:42 AM   #27
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I really haven't looked into Kevins products...I would be interested to know more about them. Granted our pH stays pretty close to constant at 7.4....but it is very possible that the stresses of our body trying to maintain this slight alkaline pH could be some of what health problems start as. Eating acidic foods may put undue stresses on the body to maintain proper pH.

I was sure you had not heard of Barrett's dealings....sometime in the not to distant future i will create a thread in the health forum dedicated to *quackwatch*.

You said-

Now as for the HIV antibody test If you do recall our last discussion I spoke of NAT or Nucleic Acid testing which tests the virus at the RNA level.

This is circular logic. Just what makes you think that the virus you speak of is so called HIV?

The only way to tell if a virus is present is to run density gradient purification/isolation. This is mandatory in identifying viral particles. This proceedure was discussed at the Pasteur Institute amongst virologists in 1971-1972 as being *the* way of isolating viruses. Even Montegnier and other virologists have cited this in their work on other retroviruses. Why is it that they used it on other retroviruses and isolated them but not HIV? They have even admitted to not being able to isolate HIV.

If HIV is the cause of AIDS then this HIV (which has never been proven to exist) must be present in all cases of AIDS, thus fullfilling at least one criteria of Koch's Postulates. However it is not.

The aforementioned Dr. Deusbrg has found thousands of cases where people had AIDS w/o being positive on a crappy HIV antibody test (read his book *Inventing the AIDS virus*). In fact this AIDS with no HIV is called *idiopathic t-cell lymphocytopenia*. Idiopathic means *disease of unknown origin*. And, according to an abstract i read from Japan as much as 3% of the population may have this *ICL*.

Take a look at Gallo's papers that were published in May 1984 in Science. These papers are the most rigorous in regards to so called HIV. They only found presence of so called HIV in 36% of AIDS patients. What caused AIDS in the other 64%? And...Gallo only found p41 as *proof* of HIV....however not a single researcher today values p41 because it is a cellular componet (actin I believe) of most or all cells.

Recently a friend was asking me some technical info about hydrogen peroxide-we are doing an ironlife interview about H2O2 and its usefullness in medicine. You know, stuff like cross linking of DNA and Superoxide Dismutase, etc....I found some interesting info-

As you are aware I am running an experiment on no fewer than 2 people that are so called HIV positive as we try to achieve HIV negative status. We are set for beginning in June. Of course H2O2 therapy along with Ultraviolet Blood irradiation are going to be used on these people, in addition to herbal med, acupuncture, detox, nutritional improvement etc....

Look what i found as I researched some of the questions for the interview-

Life Science Universal AIDS CURE
from Townsend Letter for Doctors, August/September 1995, pp. 52-61.

After 10 years of clinical experience with 165 AIDS patients, H.E. Sartori, M.D., and H. Hugh Fudenberg, M.D., conclude that treatment with ozone and a multimodal program can produce a 95% success rate in terms of normalizing laboratory test results and the physical and mental well-being of patients.

They call their AIDS treatment approach Life Science Universal (LSU) and it includes a 12-day ozone program (30-35 mg daily of ozone per 154 pounds of body weight, delivered intravenously), supplementation with vitamins, minerals, and herbs, psychological counseling, “reconditioning” (which involves a 12-step goal-setting program), internal energy exercises, and a mostly vegetarian diet with no dairy products. In an addition, they use 8 adjunctive therapies, such as homeopathy, Chinese herbs, acupuncture, coffee enemas, heat therapy, thymus extracts, and feedback control electrical stimulation (including ear acupuncture using electric currents), when needed.

Of 119 patients for whom post-treatment laboratory results were available, 53 (45%) had their T4 immune cells return to normal; other key blood factors also became normal again. For another 46 patients (39%), their T-cell count increased by at least 200.

Of 91 patients graded HIV-positive, 75% saw their conditions change to HIV-negative after completing the program. Most of the patients receiving this treatment “showed a significant improvement of their general well-being and of most of their clinical symptoms,” state Drs. Sartori and Fudenberg.

Looks like a vaccine or antivirals are no longer needed anyway. Guess we can quit dumping 7 billion a year into chasing a ghost virus,lol.

Sorry R-But you have to PROVE that what you claim to be HIV is in fact HIV. A scientist begins that process with density gradient ultracentrifugation. Part of this process includes publishing EM's of the virus and determining that they represent morphology of such a retrovirus. So far it has not been done.

Absolutely...I would like to see the work of your mentors. I will pass that info along to the Virologists I correspond with and see what they have to say.

Don't worry about the bandwidth-Before I wrote about the HIV sham I informed Winnie and Skip that i would be doing so-and I will be more than happy to pay for the bandwidth myself.

Yes, maybe one day our paths will cross. Wouldn't everybody like to be a fly on the wall for that,lol.

Take care my friend...and Happy New Year to you and the Mrs......
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" We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake"
Dr. Kary Mullis, Nobel Prize Winner in Chemistry for inventing the Polymerase Chain Reaction

"The fact is that you can not start off with bad science and end up with good medicine"

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Old 01-06-2005, 02:02 AM   #28
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Originally Posted by xRAJAx
So as to whether it exists I think we've wasted enough of Winnie's Bandwith from our last discussion. ...


LOL...your threads are always very informative...I feel like I can go perform brain surgery after reading that thread...
Anyone can become angry - that is easy, but to be angry with the right
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Old 01-06-2005, 01:14 PM   #29
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Well let me start off by saying that if this post is out of order or logical sequence please forgive me...there is just so much to respond to I have a feeling its going to be lengthy and hopefully it will be organized enough to read through easily.

but it is very possible that the stresses of our body trying to maintain this slight alkaline pH could be some of what health problems start as. Eating acidic foods may put undue stresses on the body to maintain proper pH.

Everytime we exercise our bodies our pH changes drastically. Some have even said exercising too can be dangerous with the imbalance in pH. I still say, let you body naturally use its buffer system, rather than trying to neutralize it by other external means.

This is circular logic. Just what makes you think that the virus you speak of is so called HIV?
The only way to tell if a virus is present is to run density gradient purification/isolation. This is mandatory in identifying viral particles. This procedure was discussed at the Pasteur Institute amongst virologists in 1971-1972 as being *the* way of isolating viruses

Again, this is not the ONLY way as you say to isolate a virus. I understand that you cannot prove without a shadow of doubt that the virus we isolate is HIV using the old methods, but I hope to show you a strong correlation between the two. Retroviruses using this old method are difficult to isolate. So that's why polymerase testing as well as NAT or Nucleic Acid testing is used today to take a look at the virus at the molecular level. To refresh your memory NAT testing is technology to detect viral RNA and DNA. Anti-body tests were the first tests out, were they But they did show a correlation to those who tested positive and later developed AIDS.

The aforementioned Dr. Deusbrg has found thousands of cases where people had AIDS w/o being positive on a crappy HIV antibody test (read his book *Inventing the AIDS virus*). In fact this AIDS with no HIV is called *idiopathic t-cell lymphocytopenia*. Idiopathic means *disease of unknown origin*. And, according to an abstract i read from Japan as much as 3% of the population may have this *ICL*.

I highly doubt this would be the case with NAT testing.

If HIV is the cause of AIDS then this HIV (which has never been proven to exist) must be present in all cases of AIDS, thus fullfilling at least one criteria of Koch's Postulates. However it is not.

Lets take a look at Koch's Postulate. It states the following must be true.

1. Epidemiological association: the suspected cause must be strongly associated with the disease.

2. Isolation: the suspected pathogen can be isolated - and propagated - outside the host.

3. Transmission pathogenesis: transfer of the suspected pathogen to an uninfected host, man or animal, produces the disease in that host.

For postulate #1 numerous studies across the world have shown that nearly all AIDS patients are HIV seropositive. And this number will be even better represented when the eastern world takes hold of Nucleic Acid Testing

For postulate #2: Modern nucleic testing has allowed to isolate various HIV genes in almost all patients with AIDS.

Regarding postulate #3: It has been fulfilled in tragic incidents involving three laboratory workers with no other risk factors who have developed AIDS or severe immunosuppression after accidental exposure to concentrated, cloned HIV in the laboratory. In all three cases, HIV was isolated from the infected individual, sequenced and shown to be the infecting strain of virus. In another tragic incident, transmission of HIV from a Florida dentist to six patients has been documented by genetic analyses of virus isolated from both the dentist and the patients. The dentist and three of the patients developed AIDS and died, and at least one of the other patients has developed AIDS. Five of the patients had no HIV risk factors other than multiple visits to the dentist for invasive procedures (O'Brien, Goedert. Curr Opin Immunol 1996;8:613; O'Brien, 1997; Ciesielski et al. Ann Intern Med 1994;121:886).

In addition, through December 1999, the CDC had received reports of 56 health care workers in the United States with documented, occupationally acquired HIV infection, of whom 25 have developed AIDS in the absence of other risk factors. The development of AIDS following known HIV seroconversion also has been repeatedly observed in pediatric and adult blood transfusion cases, in mother-to-child transmission, and in studies of hemophilia, injection-drug use and sexual transmission in which seroconversion can be documented using serial blood samples (CDC. HIV AIDS Surveillance Report 1999;11[2]:1; AIDS Knowledge Base, 1999). For example, in a 10-year study in the Netherlands, researchers followed 11 children who had become infected with HIV as neonates by small aliquots of plasma from a single HIV-infected donor. During the 10-year period, eight of the children died of AIDS. Of the remaining three children, all showed a progressive decline in cellular immunity, and two of the three had symptoms probably related to HIV infection (van den Berg et al. Acta Paediatr 1994;83:17).

Koch's postulates also have been fulfilled in animal models of human AIDS. Chimpanzees experimentally infected with HIV have developed severe immunosuppression and AIDS. In severe combined immunodeficiency (SCID) mice given a human immune system, HIV produces similar patterns of cell killing and pathogenesis as seen in people. HIV-2, a less virulent variant of HIV which causes AIDS in people, also causes an AIDS-like syndrome in baboons. More than a dozen strains of simian immunodeficiency virus (SIV), a close cousin of HIV, cause AIDS in Asian macaques. In addition, chimeric viruses known as SHIVs, which contain an SIV backbone with various HIV genes in place of the corresponding SIV genes, cause AIDS in macaques. Further strengthening the association of these viruses with AIDS, researchers have shown that SIV/SHIVs isolated from animals with AIDS cause AIDS when transmitted to uninfected animals (O'Neil et al. J Infect Dis 2000;182:1051; Aldrovandi et al. Nature 1993;363:732; Liska et al. AIDS Res Hum Retroviruses 1999;15:445; Locher et al. Arch Pathol Lab Med 1998;22:523; Hirsch et al. Virus Res 1994;32:183; Joag et al. J Virol 1996;70:3189).

I'll follow this post with the article my colleagues published on their methods of producing the HIV vaccine. As you know this is the project I worked on for the past 3 years. But to better understand the article and the use of the Gag pol and Gag Env of the HIV vaccine I'll give you a background on these items.

Polymerase Chain Reactions allowed scientists to take a look at the virus genes, and DNA backbone. Basically application of PCR to the study of HIV-1 infection facilitated the cloning, sequencing, and manipulating of HIV-1 genes and thereby greatly accelerated the pace of discovery. Much later after this discovery, after isolating varios genes of the virus, scientists cloned these proteins using recombinant technology. These proteins are what we use to attach to poly-lactic-co-glycolid polymers to illicit immune responses in animals and patients. So far as I spoke of before the response looks good. The idea is to have the body illicit a high anti-body response to these fragments of the virus gene which will theoretically vaccinate that patient.

Anyhow, I am looking forward to your results using H2O2. I wish you the best, and recommend that after treatment the patients use a NAT type test to test for the virus. It would wonderful for them to test negative and I wish you all the best. The brand name is Procleix system. If you need , I might even be able to have our company donate some for use.


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Old 01-06-2005, 01:23 PM   #30
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I'll include references to this article as there are many others written by these authors that might interest you or your friends. I don't think its necessary to post them all here.
__________________________________________________ _______________

Mucosal immunization with HIV-1 gag DNA on cationic microparticles prolongs gene expression and enhances local and systemic immunity

Manmohan Singh, Michael Vajdy, , Jason Gardner, Maylene Briones and Derek O’Hagan

Chiron Corporation, Immunology and Infectious Diseases, 4560 Horton Street, Emeryville, California, CA 94563, USA

Received 20 March 2001; revised 22 June 2001; accepted 9 July 2001 Available online 16 October 2001.

There is an urgent need to develop vaccines against transmission of HIV through the vaginal and rectal mucosa. In the present study we tested the ability of DNA encoding HIV-1 gag adsorbed onto the surface of cationic polylactide co-glycolide microparticles (PLG–DNA) to induce local and systemic gag-specific immunity following mucosal delivery. We found gag-specific cell- and antibody-mediated responses in local as well as systemic lymphoid tissues following intranasal (IN) immunizations with PLG–DNA but not with naked DNA. IN immunizations with PLG–DNA, but not naked DNA, induced prolonged expression of gag protein in local and systemic lymphoid tissues. These data have important implications for DNA vaccine development.

Author Keywords: Mucosal delivery; PLG-cationic microparticles; DNA vaccines

Article Outline
1. Introduction
2. Materials and methods
2.1. Mice and cell lines
2.2. Materials
2.3. Immunizations
2.4. Sera and tissue collection
2.5. 51Cr-release CTL assay
2.6. ELISPOT assay
2.7. ELISA assays
2.8. Immunohistochemistry
3. Results
3.1. Mucosal immunization with PLG–DNA enhances HIV-specific local and systemic CTL responses
3.2. Enhanced HIV-specific local and systemic humoral responses following mucosal immunization with PLG–DNA
3.3. HIV-1 gag protein expression in local and systemic lymphoid tissues following IN immunizations with PLG–DNA
4. Discussion

1. Introduction
There is an urgent need for the development of a safe, effective, and inexpensive vaccine against HIV infection. The majority of HIV infections currently occur through heterosexual intercourse, by transmission through the vaginal mucosa [1 and 2]. Accumulated evidence suggests an important role for systemic cell-mediated immune responses against HIV-1 gag in the control of infection and protection against AIDS [3, 4, 5 and 6]. However, presence of SIV/HIV-specific cytolytic T-lymphocytes (CTL) throughout the vaginal/uteral mucosa at the site of viral entry, as well as in the draining lymph node (LN) is also well-documented and this may be associated with protection [7, 8, 9, 10, 11, 12 and 13]. Therefore, a successful HIV vaccine will most likely need to elicit long-term cell-mediated immunity at sites of viral entry at vaginal mucosa and the draining LN, as well as systemically.

It is well established that mucosal immunization is the most effective means to induce long-term immunity at local and distant mucosal lymphoid tissues [14, 15 and 16]. Moreover, mucosal immunization also can induce systemic immune responses and has important advantages over parenteral immunization, including ease of administration and the avoidance of the use of needles. Therefore, the development of vaccines for mucosal administration is an important objective. The intranasal (IN) route of administration offers a practical and effective means to induce local and distant mucosal immunity in the nasal and upper respiratory mucosa and the draining LN, as well as the vaginal mucosa [17, 18, 19 and 20]. Moreover, compared to oral immunization IN immunization generally requires less antigen and induces more potent responses, particularly in genital mucosal tissues [21 and 22].

Although traditional vaccines have comprised proteins, live attenuated viruses, or killed bacteria, much attention has recently been focused on DNA vaccination. Immunization with DNA has several advantages over immunization with proteins, including the induction of CTL responses in laboratory animals and in some instances in human. The ruggedness and relative simplicity of DNA offers the potential for improved vaccine stability, and reduced costs for vaccine production. Moreover, compared to attenuated viruses as delivery vehicles for HIV genes, plasmid DNA offers a safe alternative. Clinical trials involving intramuscular (IM) immunization with DNA vaccines have already been performed in humans and the vaccines appear to be generally safe and well-tolerated at the doses tested [23, 24 and 25]. However, although DNA immunization has proven very potent in small-animal models, the potency in primates, including humans, has been variable. Consequently, there is a clear need to improve the potency of DNA vaccines for human immunization. We recently described the development of novel positively charged PLG microparticles with adsorbed DNA, which were used to induce enhanced immune responses following IM immunization [26]. PLG microparticles are a biodegradable and biocompatible delivery system, and have been safely used in humans for a wide range of biomedical purposes, including the controlled release of peptide and protein drugs [27 and 28]. In addition, PLG microparticles have been used as vaccine delivery systems for both systemic and mucosal vaccines [29].

In the current study, we explored the potential of cationic PLG microparticles to induce local and systemic cell-mediated immunity following IN immunization with DNA encoding HIV-1 gag. In addition, we measured local and systemic gag-specific antibody responses. Moreover, to investigate a possible mechanism for the enhanced immune responses induced following IN immunizations with PLG–DNA, we localized the cells that express gag protein in local and systemic lymphoid tissues.

2. Materials and methods
2.1. Mice and cell lines
Female CB6F1 (H-2b×d from an F1 cross between H-2b C57BL/6 and H-2d BALB/c) or Balb/c mice were purchased from Charles River Breeding Laboratories and were 6–8-week-old at the onset of the studies. The fibroblast cell line SvBalb (H-2d) was used as target cells. This cell line expresses class I but not class II MHC molecules, and is therefore directed against CD8+ but not CD4+ cells.

2.2. Materials
The p7g is an H-2Kd restricted HIV-1SF2p24gag CTL epitope and is a synthetic 9 mer peptide (aa, 199-AMQMLKETI-207). This peptide was synthesized with free amine N-termini and free acid C-termini using Fmoc solid-phase methods by Research Genetics (Huntsville, AL). The polylactide-co-glycolide (PLG) polymers were obtained from Boehringer Ingelheim (USA). The PLG polymer used in this study was RG505, which has a co-polymer ratio of 50/50 and a molecular weight of 65 kDa (manufacturer’s data). The HIV-1 pCMVkm p55 gag plasmid was obtained by transforming Escherichia coli strain HB101 with the plasmid and fermenting under defined growth conditions. The final product was endotoxin free (<2.5 EU/ml). The pLUC plasmid was also similarly purified. All other chemicals and reagents were obtained from Sigma Chemical Co. (St. Louis, MO), and used as shipped. The PLG/CTAB microparticles with adsorbed DNA were prepared and analyzed as described previously [26].

2.3. Immunizations
Groups of five mice were used for each immunization and tissues were pooled following sacrifice. IN immunizations were performed with PLG–DNA or naked DNA (100 g) in 25–50 l of saline. IN immunizations were performed without anesthesia four times at 2–3 week intervals, and the mice were sacrificed 1 week following the final immunization.

2.4. Sera and tissue collection
Mice were bled through the retro orbital plexus 1 day prior to sacrifice and the sera separated for ELISA assays. Nasal washes were performed by flushing 300 l PBS through the nares of anesthetized mice 1 day prior to sacrifice. Cervical lymph nodes (CLN) and spleens (SP) were harvested and pooled from five mice per group and single-cell suspensions were prepared by meshing through steel or nylon meshes.

2.5. 51Cr-release CTL assay
Spleens from immunized mice were harvested 3 weeks following a single immunization and used as pools of five. Spleen cells were cultured in a 24-well dish at 5×106 cells per well. Of these cells, 1×106 were sensitized with synthetic p7g peptide (amino acids 194–213) at a concentration of 10 M for 1 h at 37°C, and then washed and co-cultured with the remaining 4×106 untreated cells. The cells were stimulated as a bulk culture in 2 ml of splenocyte culture medium: RPMI 1640 with 100 mM -glutamine (Gibco, Grand Island, NY)/(minimum essential medium (MEM) alpha medium with -glutamine, deoxyribonucleosides or ribonucleosides) (1:1) supplemented with 10% heat-inactivated fetal calf serum (Hyclone, Logan, UT), 100 U/ml penicillin, 100 g/ml streptomycin, 10 ml/l of 100 mM sodium pyruvate, and 50 M 2-mercaptoethanol. In addition, 5% Rat T-Stim IL2 (Rat T-Stim; Collaborative Biomedical Products, Bedford, MA) was used as a source of IL2 and was added to the culture media just before the cells were to be cultured.

After a stimulation period of 6–7 days, the cells were collected and used as effectors in a chromium 51Cr-release assay. Approximately 1×106 SV/Balb target cells were incubated in 200 l of medium containing 50 Ci of 51Cr and with the correct peptide p7g, or a mismatched cell–target pair as the negative control, at a concentration of 10 M for 60 min and washed. Effector cells were cultured with 5×103 target–cells at various effector-to-target ratios in 200 l of culture medium in 96-well tissue culture plates (round or V-bottom) for 4 h. The average cpm from duplicate wells was used to calculate percent specific release as presented here. Percentage specific release was calculated as 100×[(release by test CTL−spontaneous release/total release−spontaneous release)] — specific release from a non-relevant target (to account for non-specific activity which was 10–15% of total release). The data are presented as mean±S.D. of three independent experiments with pools of five mice per group.

2.6. ELISPOT assay
Single-cell suspensions from pooled CLN and SP from five mice per group were added onto nitrocellulose or PVDF plates (Milipore) pre-coated with monoclonal rat anti-mouse anti-IFN- antibody (Pharmingen) and blocked with complete RPMI medium at pH 7.2, containing 10% fetal calf serum, 5 mM Hepes, and antibiotics. Following overnight incubation of cells in the presence of gag-derived p7g peptide, or anti-CD3 (Pharmingen) and anti-CD28 (Pharmingen) as positive control for polyclonal T-cell activation, or media only as negative control, the plates were washed and biotinylated anti-IFN- (Pharmingen) was added in PBS/0.1% BSA/0.02% Tween (P/T) and incubated at room temperature (R/T) for 2 h. The plates were washed with P/T and incubated for 1 h at 37°C with Avidin-peroxidase (Pharmingen) at 1:1000 dilution. The plates were washed with P/T and the spots were visualized by adding DAB in Tris–HCl (pH 7.5) buffer for 30 min. The plates were washed with de-ionized H2O and air-dried. Background spots from negative control (media only) wells were subtracted from wells activated with gag-p7g peptide. The number of spots in positive control wells (polyclonally activated with anti-CD3 and anti-CD28) was 5–10-fold higher than the number of spots in wells activated with gag-p7g peptide. The spots were counted with an in-house developed automated ELISPOT reader using software from Alpha Innotech Corp. (San Leandro, CA). Two to four wells per group/tissue were counted. The data are presented as mean±S.D. of two independent experiments with pools of five mice per group and expressed as the number of gag-p7g peptide-specific IFN--secreting cells (IFNSC) per 107 mononuclear cells (MNC).

2.7. ELISA assays
Serum samples were assayed for IgG or IgA titers using a bioluminescent immunosorbant assay (BIA). ELISA plates (MicroLite obtained from Dynatech) were first coated with the p55 antigen (5 g/ml) overnight. After blocking (5% goat serum, 25 mM Tris, 10 mM EGTA, 150 mM KCl, 2 mg/ml BSA, 0.3% Tween-20, pH 7.5), plates were coated with 1:10 serially diluted serum samples in blocking buffer. The plates were developed using 1:1000 diluted Goat anti-mouse IgG or IgA biotin conjugate (EY Labs, San Mateo, CA) pre-saturated with purified mouse IgG (1 mg/ml, Sigma Chemical Co.) to reduce cross-reactivity. Plates were then incubated with 1:500 diluted streptavidin-jellyfish aequorin conjugate (SeaLite Sciences, Bogart, GA). Luminescence was triggered with 10 mM calcium acetate and measured using a luminometer (Dynatech ML3000). Quantitation was based on relative light units (RLU) representing total luminescence integrated over three seconds (arbitrary units). End point titers were determined by extrapolation of plots of logarithm of luminescence versus logarithm of dilution to two standard deviations above background. The data are presented as mean±S.D. of two independent experiments with pools of five mice per group.

2.8. Immunohistochemistry
CLN and SP were removed from mice at designated time points, embedded in OCT compound (Miles Inc., Elkhart, IN) and snap frozen in 2-methylbutane (JT Baker, Phillipsburg, NJ) chilled by dry ice. Sections (5 m) were cut using a cryostat, transferred onto glass slides, and kept at −80°C until stained. Before staining, the sections were fixed in ice-cold acetone for 10 min at room temperature. After blocking in PBS/2% BSA/1% mouse serum (Dako, CA) for 1 h, the sections were washed in PBS and stained with the antibodies designated below at 1:20 (Gag-FITC) or 1:40 (CD11b, CD11c) dilution in PBS for 2 h at room temperature. Antibodies used were: anti-gag-FITC (KC57, Coulter, FL), gag-isotype-FITC control (MsIgG1, Coulter), CD11b-PE (M1/70, Pharmingen). Stained sections were mounted in Fluorsave (Calbiochem, CA) and photographed using a digital camera linked to a fluorescent microscope with FITC and PE filters. The immunostaining results shown are representative of three mice per time point.

3. Results
3.1. Mucosal immunization with PLG–DNA enhances HIV-specific local and systemic CTL responses
We found strong systemic CTL responses in splenocytes from mice immunized IN with PLG–DNA, as measured by a standard Cr-release assay (Fig. 1A). In contrast, mice immunized IN with naked DNA failed to show splenic CTL responses (Fig. 1A). Importantly, we found that IN immunizations with PLG–DNA also induced strong local CTL responses in CLN of the immunized mice ( Fig. 1B), as measured by a gag epitope-specific IFN- ELISPOT assay. Moreover, we found high numbers of gag-specific IFNSC in the spleen of the IN immunized mice, confirming the systemic immune responses measured by the Cr-release assay ( Fig. 1B). Several reports have shown a strong correlation between the number of IFNSC and the number of CD8+ T-cells with lytic activity measured by the Cr-release assay [30, 31, 32, 33 and 34]. Thus, cationic microparticles serve as efficient DNA delivery systems for induction of local and systemic CTL responses following IN immunization.


Fig. 1. Local and systemic T-cell-mediated responses following IN immunizations with PLG–DNA. Mice were immunized four times IN with PLG–DNA or naked DNA encoding HIV-1 gag at 3 week intervals and sacrificed 7 days after the final immunization. Single cell suspensions from CLN and SP were prepared from pools of five mice per group. (A) Cytotoxc T-cell responses in spleens following IN immunizations with PLG–DNA (triangles) or naked DNA (squares) as measured by the Cr-release assay. The data are presented as mean percent specific lysis±S.D. of three independent experiments. (B) Local and systemic CD8+ T-cell responses in CLN and spleen as measured by the ELISPOT assay. The data are presented as the mean number of gag-specific IFNSC per 10 million MNC±S.D. of two independent experiments.

3.2. Enhanced HIV-specific local and systemic humoral responses following mucosal immunization with PLG–DNA
There is strong evidence that protection against HIV may be mediated by both arms of the immune system, cell-mediated [3, 4, 5 and 6] as well as humoral [35, 36 and 37]. Because we detected strong cell-mediated responses following immunizations with PLG–DNA, we next sought to determine the extent of the humoral responses in local and systemic lymphoid tissues. Following IN immunizations with PLG–DNA, we found p55-specific antibody-secreting cells in local (CLN) and systemic (SP) lymphoid tissues, as measured by an ELISPOT assay ( Fig. 2A). Moreover, we detected p55-specific IgG (Fig. 2B) antibody titers in the sera of the IN immunized animals by an ELISA. However, although enhanced anti-gag serum IgA titers were detected ( Fig. 2C), no anti-gag IgA could be demonstrated in nasal secretions (data not shown). Thus, IN immunizations with PLG–DNA expressing HIV-gag induced specific local humoral responses in CLN as measured by ELISPOT and systemic humoral responses as measured by ELISPOT and ELISA.

Fig. 2. Local and systemic humoral responses following IN immunizations with PLG–DNA compared to naked DNA. Mice were immunized four times IN with PLG–DNA or naked DNA encoding HIV-1 gag at 3 week intervals and sacrificed 7 days after the final immunization. Single cell suspensions from CLN and SP or sera were prepared from pools of five mice per group. (A) Local and systemic humoral responses in CLN and spleen as measured by the ELISPOT assay. The data are presented as the mean number of ASC per 10 million MNC±S.D. of two independent experiments. (B) Serum IgG responses as measured by a chemiluminescence ELISA assay. The data are presented as mean chemiluminescent serum IgG titers from pools of five mice per group±S.D. of two independent experiments. (C) Serum IgA responses as measured by a chemiluminescence ELISA assay. The data are presented as mean chemiluminescent serum IgA titers from pools of five mice per group±S.D. of two independent experiments.

3.3. HIV-1 gag protein expression in local and systemic lymphoid tissues following IN immunizations with PLG–DNA
In order to investigate a possible mechanism for the enhanced immune responses following In immunizations with PLG–DNA, we determined the magnitude of gag protein expression in local and systemic lymphoid tissues at 1 and 7 days following a single IN immunization with PLG–DNA versus naked DNA. By immuno-fluorescent staining on frozen sections, we found that, at 1 day after immunization with PLG–DNA many cells expressed gag in CLN and SP, while it appeared that fewer cells expressed gag after immunization with naked DNA (Fig. 3 and Fig. 4). In contrast, at 7 days following a single IN immunization, mice immunized with PLG–DNA had many cells expressing gag both locally in CLN as well as systemically in SP, while mice immunized with naked DNA had no cells expressing gag in CLN or SP (Fig. 3 and Fig. 4). These data show that, following IN immunization with PLG–DNA versus naked DNA, over time, more cells express the encoded protein for prolonged periods of time in local and systemic lymphoid tissues.

Fig. 3. Duration of expression of gag antigen in CLN from mice immunized with naked DNA or PLG–DNA encoding HIV-1 gag. Tissues were removed either at 1 day (left side, panels A, C, E) or 7 days (right side, panels B, D, F) following IN immunization with buffer alone (A, B), naked DNA (C, D) or PLG–DNA (E, F). Immunohistochemical staining with anti-gag FITC antibody was performed as described in Section 2.

Fig. 4. Duration of expression of gag antigen in spleen from mice immunized with naked DNA or PLG–DNA encoding HIV-1 gag. Tissues were removed either at 1 day (left side, panels A, C, E) or 7 days (right side, panels B, D, F) following IN immunization with buffer alone (A, B), naked DNA (C, D) or PLG–DNA (E, F). Immunohistochemical staining with anti-gag FITC antibody was performed as described in Section 2.

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4. Discussion
In the current studies, we demonstrated that a novel approach for IN immunization using cationic PLG microparticles with adsorbed DNA induced enhanced local and systemic cell-mediated, as well as humoral, immunity against HIV-1 gag. In addition, we localized the cells that expressed gag and we proposed a possible mechanism for the enhanced immune responses observed.

We found a clear enhancement of local gag-specific antibody-secreting cells (ASC) in CLN following IN immunizations with PLG–DNA versus naked DNA.

The enhancement of systemic responses in spleen as measured by ELISPOT was less clear in spleen and the response in spleen was generally low in both groups of animals. However, by luminometry ELISA, we detected high titers of gag-specific IgG antibodies in serum of mice immunized with PLG–DNA but not in mice immunized with naked DNA. Moreover, we did not detect any IgA antibodies in nasal secretions. We hypothesize that this observation is due to the general difficulty in inducing humoral responses against HIV gag or env antigens compared to other antigens, e.g. influenza HA (unpublished observation). We also attribute the discrepancy between serum ELISA and spleen or CLN ELISPOT data to the sensitivity of the luminometry ELISA assay and the ELISPOT assay as well as to the fact that serum antibodies, besides spleen, stem from other tissues such as bone marrow.

In previous studies involving mucosal immunization with DNA, the DNA has been formulated with adjuvants and delivery systems to enhance immunogenicity [38, 39, 40, 41 and 42]. However, the DNA delivery formulations used in these studies were often not fully characterized and were of unknown toxicity [38, 39 and 40]. Moreover, in some studies, the encoded model antigens were not related to infectious diseases [40 and 41]. In addition, although in some of these reports enhancement of immune responses was observed, often only systemic humoral or cell-mediated immunity was measured and no local immune responses were reported [41 and 42].

In the current studies we described the use of a biodegradable and biocompatible polymer for DNA delivery, PLG, which has already been approved as a component of a number of drug delivery systems and has a long history of safe use in humans [43]. Mathiowitz et al. previously described the use of microparticles for mucosal DNA delivery, but reported only on expression of a marker gene entrapped in microparticles, and no immune responses were reported [44]. Jones et al. described the use of PLG microparticles as an oral delivery system for a DNA vaccine, but described only antibody responses to a marker gene, which was not an infectious disease related antigen [41]. Nevertheless, Chen et al. subsequently showed that PLG microparticles with entrapped DNA could be used to induce protective immunity against viral challenge in mice. However, again only low levels of humoral immune responses were reported and cell-mediated immunity was not described [42]. Importantly, although PLG microparticles appear to have significant potential for mucosal delivery of DNA, the formulations previously described had serious limitations. For example, recent work has confirmed our own observations and shown that DNA is significantly damaged following microencapsulation in PLG microparticles, due to exposure to high shear during particle preparation [45, 46 and 47]. It has been reported that microencapsulation of DNA results in a significant reduction in the amount of supercoiled DNA, with only 10–20% of the encapsulated material retaining super-coiled structure [45 and 47]. Moreover, encapsulation efficiency of DNA in microparticles is low, with only 20–50% encapsulation efficiency reported [45 and 47].

To overcome these and other significant problems, we developed the novel approach of adsorbing DNA onto the surface of microparticles. In contrast to the observations reported for microencapsulated DNA, adsorption of DNA to cationic microparticles results in maintenance of super-coiled DNA and allows a high efficiency of DNA association with PLG [26]. These important advantages of the adsorption approach, including enhanced DNA stability and formulation loading efficiency, make this process much more amenable to commercial development. Notably, the current paper describes for the first time the successful application of PLG microparticles for IN delivery of DNA, since all previous reports have described oral delivery [41, 42 and 44]. This is a particularly important observation in relation to local protection against HIV infection, since it has previously been reported that IN immunization in primates, including humans, induces potent immune responses in the genital tract [17 and 48]. In contrast, oral immunization is relatively inefficient for the induction of genital tract immune responses [48]. Importantly, it has been reported that CTL responses in the genital mucosa play a role in protection against heterosexual transmission of HIV-1 in humans [13]. Subsequent studies using cationic PLG microparticles with adsorbed DNA will directly assess the ability of mucosal immunization to induce CTL responses in the genital mucosa. In this respect, the current observations of local CTL responses following local immunization with PLG–DNA are very encouraging.

Little information is available regarding the mechanisms of DNA uptake and expression following mucosal delivery. In our immunostaining studies of spleen, we found that 1 day after IN immunizations with PLG–DNA, the majority of gag-expressing cells were CD11b+ (data not shown) suggesting that this cell population may be responsible for uptake and expression of DNA. It is important to note that, although previous studies have suggested an important role for dendritic cells (DC) for uptake and expression of encoded protein following IM DNA injection [49 and 50], there are distinct differences in the anatomy, structure, and cellular constituents of nasal and upper-respiratory mucosa compared to muscle. The most important of these distinctions may be the presence of M-cells overlying the nasal-associated lymphoid tissue (NALT) [51, 52 and 53]. It is well established that M-cells are highly efficient in the uptake of particulate antigens and microparticles and delivery to underlying antigen-presenting cells (APC) in the local lymphoid structure [54, 55 and 56]. Although not directly addressed in our study, adsorbing DNA–PLG microparticles may enhance the uptake of DNA into NALT by M-cells. Studies are underway to characterize the cells in NALT that are involved in the initial uptake and expression of DNA and their migration pattern to mucosal and systemic lymphoid tissue.

Although CD11b is expressed by many cell populations, it is primarily considered a marker for tissue macrophages (Macs) and DC, which are both professional APC [57, 58 and 59]. However, compared to Macs, DC are more potent APC [60 and 61]. Our data suggest that monocyte lineage cells, Macs and/or DC, are involved in the uptake and expression of gag-DNA, since we detected both CD11b+ and CD11c+ gag-expressing cells. Whether these cells also actively present gag peptides to neighboring naïve T-cells in vivo is an important issue and needs further investigation. Our previous in vitro data showed that bone marrow-derived DC can take up PLG–DNA encoding HIV-1 gag and present it to a gag-specific T-cell hybridoma (Denis-Mize et al., unpublished observations).

Although uptake of cationic PLG into NALT and delivery of the adsorbed DNA–APC is likely to be an important component of the enhanced immune responses observed here, there may be other contributing factors involved. For example, the prolonged expression of DNA following IN immunizations with PLG–DNA may be in part due to protection of DNA from damage by tissue DNAse, which has previously been reported in vitro [26]. In addition, the presence of the cationic surfactant, CTAB, on the surface of PLG microparticles may contribute to disruption of endosomes and subsequent release of DNA into the cytoplasm, to enhance the response. Elucidation of these and other possible factors that contribute to the enhanced responses observed following IN delivery of PLG–DNA versus naked DNA is under further investigation.

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Old 01-06-2005, 01:25 PM   #32
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Originally Posted by winnie
LOL...your threads are always very informative...I feel like I can go perform brain surgery after reading that thread...

Thanks bro, now I don't feel so bad about those long ass


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Old 01-06-2005, 09:52 PM   #33
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Responding to your first post-R-

Again, this is not the ONLY way as you say to isolate a virus. I understand that you cannot prove without a shadow of doubt that the virus we isolate is HIV using the old methods, but I hope to show you a strong correlation between the two. Retroviruses using this old method are difficult to isolate. So that's why polymerase testing as well as NAT or Nucleic Acid testing is used today to take a look at the virus at the molecular level. To refresh your memory NAT testing is technology to detect viral RNA and DNA. Anti-body tests were the first tests out, were they But they did show a correlation to those who tested positive and later developed AIDS.

The density gradient ultracentrifugation technique is the accepted method of viral isolation. Virologists all over the world still use it. The rules for isolation are as follows-

1. Culture putatively infected cells.

2. Purify a sample in a sucrose density gradient.

3. Photograph the 1.16 band proving there are particles of the right size and form, and there is no other material.

4. Extract and analyse the constituents of the particles and prove they contain reverse transcriptase by showing they can make DNA from RNA.

5. Culture purified particles with virgin cells demonstrating that a new set of particles appears with the same morphology and constituents as the originals.

All of the major players in HIV research have used this method for many decades. Montegnier and Barre Sinoussi I know have cited this in their isolation attempts with other viruses. Gallo and Deusberg also use this technique, as does The Perth Group from Australia which is led by Dr Val Turner and Dr. Eleopulos. I have jad email contact with Dr. Turner, and according to him, this is the most reliable and accepted way of isolating viruses.

The reason I am (along with thousands of others) are so hung up on the isolation issue is that this is how a *gold standard* is developed-a blueprint of the virus. To date, there is no gold standard, and this is recognized by the US government and the antibody test kit manufactures. This is why I question the genetic material that you have referred to as *HIV*. Even the FDA agrees that there is no gold standard.....hence they do not authorize these antibody kits to be used by doctors to diagnose anyone with HIV. There are no fewer than 36 HIV antibody test kits on the market and not a single one is FDA approved to test anyone for HIV. PCR is not authorized either. However MD's do this all the time.

My point is this-you are using nucleic acid testing to find genetic material that is supposed to be HIV. However, without a blueprint of the genetic material it is not possible to identify it as HIV. Basically, what it amounts to is researchers extracted an adenosine rich strand of genetic material from cell cultures and claimed it was HIV even though they had no visual proof from electron microscopy that this is true.

Concerning PCR even the inventor of it (Dr. Kary Mullis, Nobel Winner for his invention of PCR) says his device is incapable of any use in HIV technology. Because there is no *gold standard*, no blue print.

Even the ProHIV camp can not agree as to how many genes this so called HIV has. In 1988 they said it had 8 genes. In 1990 they said it had 10 genes. In 1996 Montegneir said it had 8 genes. According to Barre' Sinoussi HIV has 9 genes. Not even the number of nucleotides of HIV genome seems to be constant (Eleni Papadopulas Eleopulos, Val Turner, John M. Papadimitiour, David Causer-The Isolation of HIV-Has It Really Been Achieved? , Continuum Sept/Oct 1996 , 4(3)5:1-24

If HIV were truly isolated it would be no problem in examining how many genes it has.

True-retroviruses are difficult to isolate and purify. More than one scientist has put forward that they are not viruses at all. They are in fact part of the human genome and are passed down from mother to child. According to these scientists these retroviruses were called *viruses* because they transcribe their genetic material backwards-this is not normal compared to other cells, so they assumed it was a virus. More on that some other time.

True that people that test HIV positive usually go on to develop AIDS. That is relatively easy to explain.

The reason people test positive on an HIV antibody test has nothing to do with HIV. These tests are not specific for so called HIV antibodies. It is well known that these tests cross react with at least 66 other items such as hep B vaccine, carbohydrate complexes, pregnancy, flu viruses, etc...

With an antibody test such as the HIV one there is a threshold that has to be met. These tests are not *yes or no*. They are *maybe*. They are not black and white-they are grey. It is likely that we all have these antibodies that are so called HIV antibodies. And this is probably why people test positive-

As cell mediated immuntiy fails for whatever reason (malnutrition, drug usage, multiple exposures to microbes, etc) antibody levels in general tend to rise. As these levels rise it increases one's chances of testing positive on a non-specific antibody test such as the *HIV test*. This is hypergammaglobulinemia.

This is why the majority of people that test positive are these people-

Third world poor-these people are malnuorished and combat tropical type diseases such as typhoid, tuberculosis, parasitic infections, dengue fever, etc. Many people in sub sahara Africa literally drink fecal matter that is in their water. It is impossible for the immune system to operate normally in this condition. Hence they develop AIDS.

Drug Abusers-Drug abuse was the first to be implicated in AIDS. It was called GRID back then, and it's cause was due to drug usuage-particularly cocaine and nitrate poppers. These drugs were the rage amongst gay males of yesteryear. The effects of nitrates are well documented-they oxidize the blood and this in facts compromises cell mediated response.Gay males that partake as a reciepient of anal intercourse is at serious risk of devloping AIDS. Many of the lubricants are polluted with benzene , a known toxin that accumalates in the thymus-this is where t cells are made. Benzene also is harmful to the bone marrow where red cells are made. W/o proper hemoglobin activity oxygen transport and uptake is impossible. Our granulocytes-a key immune cell of cell mediated response-uses up to 100 times as much oxygen for the respiratory burst as the cells use in respiration. With not enough oxygen available cell mediated response fails. It is also known that the rectal lining is very delicate-during anal intercourse it is likely that bacteria will enter the receipients blood-more immune problems. Sperm is also very immunosupressive when entering the bloodstream.

All of this considered-drug consumption and anal intercourse-it is no suprise that immunity fails and as antibody levels rise the HIV *test* will react positively.

AZT users-

AZT is a chemotheraputic drug that is calssified as a DNA chain terminator. It was developed in the 1960's for cancer patients but was denied approval because it was too toxic. It killed people. But yet with the advent of this HIV pseudoscience it was rapidly approved for people with nothing more than the presence of so called HIV Antibodies.

Cancer drugs are usually designed to target the quickest multiplying cells-which is what tumors are really. The quickest multiplying cells in the body are in the digestive system, bone marrow, and muscle tissue. Practically all people deemed HIV positive that use AZT demonstrate massive diarrhea, muscle wasting, and low red cell counts. Also key immune cells are made in the bone marrow. W/o properly assimilating food and nutrients these people can not experience proper immune functioning. Again, with the bone marrow being crushed not enough oxygen is available for the repiratory burst...which is our first line of defense against cancerous cells and invaders.

Take a gay male that abuses drugs and he will certainly end up testing positive sooner or later and then put him on AZT....well no wonder he dies.

The longest surviving *HIV* patients are ones who choose not to use antivirals in the form of AZT and it's analogues.

Lets take a look at Koch's Postulate. It states the following must be true.

1. Epidemiological association: the suspected cause must be strongly associated with the disease.

2. Isolation: the suspected pathogen can be isolated - and propagated - outside the host.

3. Transmission pathogenesis: transfer of the suspected pathogen to an uninfected host, man or animal, produces the disease in that host.

Does HIV satisfy Koch's Postulates? It fails miserably.

Let's talk about what AIDS really is. AIDS is the collapse of the immune system due to a key subgroup of cells that are in lower numbers than what are supposedly normal. These cells are the CD-4 lymphocytes, aka t-4 cells, aka t-cells. The Pro HIV mindset is that HIV causes their destruction, and HIV only. There is absolutely nothing else that can cause this destruction of CD-4's. This means that HIV would appear in each and every case of AIDS, and in sufficient quantities to cause the loss of cd-4's. But there is a huge problem with this thinking.

Growing numbers of cases of severe immune suppression have been reported that are clinically identical to AIDS, but do not test positive for HIV. *Because HIV is not present these cases are not registered as AIDS.* The CDC's rationale is simple-HIV causes AIDS, and if no HIV is present then it can not be AIDS.
Although several hundred cases of HIV negative AIDS have been documented in the medical literature for years, it was not until the International AIDS Conference in Amsterdam in July of 1992 that the world media acted with alarm, criticising the CDC for not taking the *handful* of cases more seriously. A single abstract written by an American doctor in regards to 6 cases of AIDS with no HIV sparked many other docs to come forward with their own cases that fit the same description.
The CDC quickly settled on a new name for this disease-idiopathic t-cell lymphocytopenia (ICL).
Dr. Peter Deusberg did some research on this AIDS with no HIV and he found over 6,000 cases of it here in the US. more people that are not so called HIV positive got their cd-4 cell counts taken it was found that lots more people have low t-cell counts without HIV than there are people with low t-cell counts with HIV.
Before I post this article about ICL I do want to mention that Dr. Montegnier-who was the one that initially discovered what is called HIV has said from the beginning-1982-that AIDS is a multifactoral disease and that *HIV* may play a part...but no one will develop AIDS with out these other co-factors.

More on ICL-
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" We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake"
Dr. Kary Mullis, Nobel Prize Winner in Chemistry for inventing the Polymerase Chain Reaction

"The fact is that you can not start off with bad science and end up with good medicine"

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Old 01-06-2005, 09:57 PM   #34
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A variety of causes and their implications to a multifactorial model of AIDS
By Matt Irwin

Feb. 2001


Low CD4+ T lymphocyte counts (CD4 counts) are associated with a variety of conditions, including many viral infections, bacterial infections, parasitic infections, sepsis, tuberculosis, coccidioidomycosis, burns, trauma, intravenous injections of foreign proteins, malnutrition, over-exercising, pregnancy, coricosteroid use, normal daily variation, psychological stress, and social isolation. There are also a number of people who are completely healthy and who have low CD4 counts for no apparent reason.

This paper presents a brief review of several studies documenting low CD4 counts in people who are experiencing these conditions. Low CD4 counts are so common that this undermines the most fundamental claim about HIV, which is that HIV causes low CD4 counts. The vast majority people diagnosed HIV-positive have experienced at least one of the other causes of low CD4 counts, and so there is no way to know if HIV is the cause.

The low CD4 counts caused by some of these conditions often fall below 200 per cubic millimeter, which is the level needed to diagnose acquired immunodeficiency syndrome (AIDS) in someone who was previously positive for antibodies to the human immunodeficiency virus (HIV-positive). For example, about 30% of people with acute pneumonia have been found to have CD4 counts of less than 200. In someone diagnosed HIV-positive a level below 200 is considered a sign that they have extreme immunosuppression and that HIV is destroying their immune system. Because of their low CD4 count they would be started on several antimicrobial medications to prevent infections, as well as being started on protease inhibitors and DNA chain terminators.

Because many of the conditions that cause low CD4 counts are common in people diagnosed HIV-positive, this paper advises caution regarding the use of CD4 counts to make treatment and diagnostic decisions. This is made more urgent since some of the conditions, like psychological stress, are greatly increased when people are told that their CD4 counts are low, which may cause the CD4 count to fall even further. Psychological stress and social isolation are also created by the diagnosis, HIV-positive, and by the diagnosis of AIDS, which may have chronic effects on the CD4 count. Finally, the widely accepted argument that HIV specifically targets CD4+ T lymphocytes is also called into question, because it appears that low CD4 counts are a common reaction to many kinds of physical and psychological stressors. Other alterations in immune system parameters which are thought to be specific to HIV, such as inverted CD4/CD8 ratios, are also replicated extremely well in the conditions that cause low CD4 counts, making it impossible to distinguish any effects attributed to HIV that could not also be caused by these other factors. When several of these conditions are combined in the same person, as is often the case in people diagnosed HIV-positive, extremely low CD4 counts may be a natural result.


Low CD4 T-cell counts are considered to be a marker of the progression of HIV infection and AIDS, and have been called the "hallmark" of HIV infection (Balter 1997). When Robert Gallo's team of researchers first proposed that HIV was a possible cause of AIDS, they did so because HIV was thought to infect CD4+ T-lymphocytes. They demonstrate this in the introductory paragraph of their very first HIV paper published in 1984:

"The underlying disorder affects the patient's cell-mediated immunity, resulting in absolute lymphopenia and reduced subpopulations of helper T lymphocytes (CD4+). Moreover, before a complete clinical manifestation of the disease occurs, its prodrome, "pre-AIDS", is frequently characterized by unexplained chronic lymphadenopathy [swollen lymph glands which likely indicate hyperstimulated antibody mediated immunity] or leukopenia involving helper T lymphocytes [low CD4 counts]. This leads to the severe immune deficiency of the patient and suggests that a specific subset of T-cells could be a primary target for an infectious agent." (Popovic et al 1984, page 497)

Although this claim has been repeated often since 1984, one clue that it may not be entirely accurate is that the mechanism by which HIV supposedly destroys CD4+ T-cells continues to be elusive in spite of a great deal of research looking at this question. Gallo originally claimed that it killed CD4+ T-cells as other viruses do, by direct rupturing of the cell, but this proposal had to be abandoned when it was found this did not in fact happen. Since then many different hypotheses have been presented, and a conference was called in 1997 to attempt to resolve the dispute (Balter 1997). A quote from the article by Balter (1997) which describes the conference reveals how difficult this proved to be:

"It might be said that AIDS researchers know the virus that causes the disease, HIV, inside and out. They have isolated its proteins, sequenced its genome, and identified the receptors it uses to dock onto the CD4 T lymphocytes that are the viruses primary target. Yet the central mystery of AIDS remains unresolved: How does the virus cause the severe loss of CD4 T-cells, which wrecks the immune system, that is the hallmark of the disease?" (Balter 1997, page 1399)

Since HIV was first claimed to be the cause of AIDS in 1984, the CD4 count has been widely used to make treatment and diagnostic decisions, but the use of the CD4 count has been controversial, and recommendations regarding how to use them have changed many times over the years (Goldman 2000, Hughes et al. 1998, Choi et al 1993).

In addition to low CD4 counts, the CD4/CD8 ratio is also considered a marker of disease progression in HIV and AIDS, and is often found to be inverted. An 'inverted' ratio simply means that there are less CD4 cells than CD8 cells, resulting in a ratio of less than 1. CD8 cells are often increased, especially in less advanced stages of AIDS, and this combination of lowered CD4 counts and increased CD8 counts are commonly thought to occur only in people diagnosed HIV-positive. Another finding that is common in people diagnosed HIV-positive is reduced lymphocyte activity and function, as measured by their responsiveness to foreign antigens. This can result in a state of "anergy", where people's skin fails to respond when antigens are injected under it. As this paper will demonstrate, all of these changes are common in a wide variety of conditions that commonly occur to people diagnosed HIV-positive.

There are two major arms of the immune system, one which works through antibodies, which are produced by B-cells and plasma cells, and the other that works through direct cellular action and which relies heavily on CD4+ T-cells. The first is called antibody-mediated or humoral immunity, and the second is called cell-mediated immunity. It is the cell-mediated arm of the immune system that is found to be profoundly suppressed in people diagnosed with AIDS. The antibody-mediated arm of the immune system, however, is usually hyperstimulated in the early stages, with "increasing levels of humoral antibodies and plasma cells" (Fox 1996). The fact that antibody levels are increased is what allows the HIV antibody screening tests to use serum that has been diluted 400 times, unlike other antibody tests that usually use straight, undiluted serum (Abbott Laboratories 1997). In these early stages the lymph nodes may grow in size and be chronically enlarged. In late stages, however, both the cell-mediated and antibody-mediated arms of the immune system begin to fail, and lymph node atrophy results. The only measurement commonly used in clinical practice, however, is the CD4 count, as the following treatment and diagnostic recommendations demonstrate (Cecil Textbook of Medicine, Goldman 2000):

- "Over the years, the recommendations of when to begin therapy for HIV have fluctuated back and forth, and a prior trend to treat most patients with fewer than 500 cells/mm3 with zidovudine (AZT) was modified by the results of a large randomized study (the Concorde Trial) showing that early AZT therapy did not yield improvement in survival." (Goldman 2000, page 1939)

- When the CD4 count in someone diagnosed HIV-positive is found to be below 200, AIDS is diagnosed. This method currently accounts for over half of all AIDS diagnoses, and so is highly significant (CDC 1999).

- There are two approaches regarding when to start antiretroviral therapy. The more aggressive approach recommends starting when the CD4 count falls below 500, and the second approach is to wait until it is below 350 unless the viral load is also above 20,000 copies per ml. The more aggressive approach is more commonly used in the United States, and many clinicians will even start antiretroviral medications immediately in all patients, regardless of the patient's CD4 counts.

- To prevent pneumocystis carinii pneumonia (PCP), antibiotics should be started if the CD4 count is found to be below 200. The most commonly used combination is sulfamethoxazole/trimethoprim (SMX/TMP), commonly referred to by its brand name, Bactrim.

- To prevent fungal infections, the antifungal medication fluconazole should be started if the CD4 count is below 200.

- To prevent mycobacterium avium complex (MAC) infection, the antibiotics clarithromycin, azithromycin, or rifabutin should be started if the CD4 count is below 100.

- To prevent cytomegalovirus (CMV) infection, oral gancyclovir can be started, although no CD4 level or other guideline is given.

New recommendations from the National Institute of Health were presented in February, 2001, calling for a change which would require lower CD4 counts, 350 or less, before starting antiretroviral drugs (Garrett 2001). This marks a retreat from the "hit hard, hit early" approach advocated by David Ho and others since 1996 when protease inhibitor combination therapy was begun, but it is uncertain whether clinicians are following them, with some continuing to recommend antiretroviral drugs regardless of the clinical situation.

While most people know about the lowered CD4 counts which are common in people diagnosed HIV-positive, but very few people or clinicians seem to know how common low CD4 counts are in people considered HIV-negative. Studies show that CD4 counts commonly fall extremely low, especially if a person suffers from certain conditions. These conditions include a variety of viral illnesses, bacterial infections, parasitic infections, sepsis, septic shock, multiple organ system failure, tuberculosis, coccidioidomycosis, burns, trauma, transfusions, malnutrition, over-exercising, pregnancy, normal daily variation, psychological stress, and social isolation.

In addition to lowered CD4 counts, other immune system changes occur that are also identical to those seen in people diagnosed HIV-positive, including reduced CD4/CD8 ratios, increased CD8 cells, reduced lymphocyte function, anergy, increased antibody levels, atrophy of lymphoid organs, and general suppression of cell-mediated immunity. These effects can take weeks or months to return to normal, and, if there are recurrent infections or if multiple factors are present, the low CD4 count could take much longer than this to correct, or may even stay low indefinitely. Finally, the drugs used to treat HIV commonly cause a dose dependent immunosuppression, as well as other side effects that can easily be blamed on HIV, and this has been made clear by strongly worded warnings from the drugs' own manufacturers.

A number of studies that examine these effects will be reviewed here, and studies will be emphasized if they reveal either lowered absolute CD4 counts, lowered CD4 percentages, or a reduced CD4/CD8 ratio, since these are most often thought to be specific to HIV and AIDS. This is not meant to be a comprehensive review, but rather to highlight the most significant studies on this topic.

1) Low CD4 counts in the intensive care unit

In 1995, Feeney et al. looked at CD4 counts in 102 consecutive intensive care unit (ICU) patients who were admitted for a variety of reasons, all of whom were HIV negative. The patients suffered from 34 different illnesses, with the most common being myocardial infarction (heart attack), severe bleeding, renal failure, trauma, and chronic pulmonary disease. 30% of these patients had CD4 counts less than 300, and 41% had CD4 counts less than 400. The authors do not discuss how many had counts below 200, the level resulting in a diagnosis of AIDS, or exactly how many had counts below 500, the level at which antiretroviral medications would be started in someone who has been diagnosed HIV-positive. They also did not find that low CD4 counts were linked with a poor prognosis. Here are the author's comments on their findings.

"Our results demonstrate that acute illness alone, in the absence of HIV infection, can be associated with profoundly depressed lymphocyte concentrations. Although we hypothesized that this depression would be directly related to the severity of illness, this was not seen in our results. The T-cell depression we observed was unpredictable and did not correlate with severity of illness, predicted mortality rate, or survival rate. This study was consistent with prior studies that have shown similar decreases in T-cell counts in specific subsets of acutely ill patients. These subsets included patients with bacterial infections, sepsis, septic shock, multiple organ system failure, tuberculosis, coccidioidomycosis, viral infections, burns, and trauma patients. Most of these studies reported decreases in lymphocyte populations, some of which were severe and included CD4/CD8 ratio inversions..."

"In the largest study to date of hospitalized patients, Williams et al (1983) evaluated T-cell subsets in 146 febrile patients with serious acute infections... with 19 of 45 patients having a CD4 count of less than 300 per microliter.

We also found that CD4 counts were linearly related to total lymphocyte concentrations, as Blatt et al. (1991) reported in HIV-positive patients." (Feeney et al. 1995, pages 1682-1683)

These researchers did not find that low CD4 cell counts were good measures of prognosis, although some other reports differ in this regard.

2) Low CD4 counts in Various Human Infections

2a) Pneumonia, pyelonephritis, abscesses, infected wounds, cellulitis, and sepsis

In 1983, about one year before HIV was first mentioned as a possible cause of AIDS, Williams et al. published a study showing severely reduced CD4 counts in 146 consecutive people with serious acute infections who were admitted to their hospital in New Mexico. This article was referred to in the article by Feeney et al. that was reviewed above. The infections included pneumonia, acute pyelonephritis, abscesses, infected wounds, cellulitis, deep tissue infections, and sepsis.

The authors only provide average CD4 counts for the majority of patients, except for a graph on page 811 that plots the CD4 counts for all 45 pneumonia patients. This reveals that 31 of 45 (69%) had CD4 counts less than 500 cells/mm3, 19 of 45 (42%) had counts below 300, 13 of 45 (29%) had counts below 200, 6 of 45 (13%) had 100 or less, and 2 of 45 (4%) had values less than 50. The average CD4 count for all the people with pneumonia was 574. Although CD8 cells were mildly reduced, the CD4/CD8 ratio was often inverted as seen in AIDS, and the authors caution against using CD4/CD8 ratios to evaluate AIDS patients: "we caution that because infection itself often results in helper-suppressor ratios of less than 1.0, ratios alone cannot be used to define the presence of profound acquired immunodeficiency" (Williams et al. 1983, page 815).

They provide tables with clinical information and CD4 counts for 9 patients with soft tissue infections (STI) and 12 patients with sepsis/deep infections, all of whom had multiple T-cell abnormalities. Brief descriptions of all the cases from these tables who had CD4 counts less than 200 follow:

- a 25 year-old female with "disseminated varicella", CD4 count of 58, "rapid septic course, death".

- a 41 year-old male with Group A hemolytic streptococcal sepsis, CD4 count of 150, "rapid progression, ... death".

- a 42 year-old male with E-coli sepsis, CD4 count of 156, "Multiple previous episodes of E-coli bacteremia".

- a 38 year-old female with a submandibular abscess, CD4 count of 183, "Gram-positive organism, short 5-day hospital stay".

- a 46 year-old man with peritonitis, CD4 count of 205, who was on long-term peritoneal dialysis.

- a 58 year-old female with infected decubitous ulcers, CD4 count of 189, "prolonged 4-month hospital stay, ... E-coli and pseudomonas organisms".

- 75 year-old female with a common duct stone and ascending cholangitis, CD4 count of 139, "multiple positive blood culture results".

These case examples are notable in that some of them sound very similar to people who die of AIDS, such as the 25 year old female who died of disseminated varicella with a CD4 count of only 58 cells/mm3. Others, such as the 38 year old female with an abscess and CD4 count of 189 who was released after a "short 5-day hospital stay" suggest that many people with extremely low CD4 counts can achieve quick recoveries. It is also remarkable that 30% of people with pneumonia, which is a very common illness in people diagnosed HIV-positive, had CD4 counts below 200, and 70% had counts below 500. These authors did find some correlation between severity of illness and CD4 counts; patients with sepsis who recovered also had gradual increases in CD4 counts, while those that died had counts that remained low.

2b) Low CD4 counts in malaria

Malaria is caused by parasites from the plasmodium species, and is extremely common in Africa and in many tropical areas. In 1999 a letter was published documenting severely lowered CD4 counts in African patients with malaria (Chirenda 1999). The author examined the CD4 count in 78 patients with malaria who were HIV-positive, and 19 who were HIV-negative. He was surprised to find that more HIV-negative malaria cases had severely lowered CD4 counts than did the HIV-positive cases, on average, with 8 of 19 (42%) HIV-negative cases being below 200, while only 31 of 78 (40%) HIV-positive cases had CD4 counts below 200. Seven HIV-negative malaria cases had CD4 counts below 100. This data comes from Table 1. In addition, 6 HIV-positive patients had normal CD4 counts, and the author states, "One may want to hypothesise that malaria reduces the CD4 count more than HIV infection". The author did not do statistical analyses to test for statistical significance, nor does he mention the general health or nutrition status of the patients, which may have contributed to their severely lowered CD4 counts, as will be reviewed later in this paper.

2c) Low CD4 counts in mononucleosis

Mononucleosis, commonly called 'mono', is a common viral illness, especially in young people of college age, and can last for several months. It is caused by cytomegalovirus (CMV) or Epstein-Barr virus (EBV), and usually results in prolongued cold and flu symptoms, swollen lymph nodes, and fatigue. In 1981 a group of researchers looked at CD4 and CD8 counts in ten consecutive patients with acute CMV mononucleosis, and compared their counts with those of ten healthy volunteers (Carney et al. 1981). The CD4 counts in people with mononucleosis were signifcantly reduced, with the healthy volunteers having 73% more CD4+ cells per ml than did people with mono, on average. The CD8 cells in people with mono were increased, and the combination of lower CD4 counts and elevated CD8 counts resulted in an inverted CD4/CD8 ratio in every patient. The average ratio was only 0.2, compared to the normal average of 1.7 found in controls. The CD4 counts were measured in nine of the ten patients, and the three with the lowest CD4 counts had 194, 202 , and 255 cells/mm3. The authors also found that the T-lymphocytes of people with mononucleosis responded poorly to antigens, showing depressed function. this paper was published three years before HIV was first claimed to be the cause of AIDS.

Five years later, a different set of researchers measured various lymphocyte subsets in acute EBV mononucleosis (Junker et al. 1986). They took 17 consecutive patients who had recently been diagnosed, gave them an immunization designed to activate their B lymphocytes, and then took samples of blood. The immunization makes this study different from any of the other studies to be examined here. They did not find a statistically significant lowering of CD4 counts, but they did find significantly lowered CD4/CD8 ratios due to elevated numbers of CD8 cells, with the ratios falling below 1 as commonly occurs in people diagnosed HIV-positive. They also found increased B-cell activity with excess antibody production. Although this increased antibody production is common in many of the conditions that cause lowered CD4 counts, the authors assume that the increase occurs because EBV infects lymphocytes. It appears more likely that increased antibody production is a normal response to a wide variety of physical and psychological stressors. The authors conclude that "these studies demonstrate that infection with EBV affects both B and T lymphocytes and causes a broad based transient immune deficiency in patients with uncomplicated infectious mononucleosis" (Junker et al. 1986, page 436). The immune deficiency was "transient" but long lasting, with CD4/CD8 ratios gradually returning to normal over the course of 4 to 6 weeks.

2d) Low CD4 counts in sepsis

In 1986, a group of researchers from Osaka, Japan published a study where they examined various lymphocyte subsets in 9 consecutive patients admitted to the ICU with sepsis (Nishijima et al. 1986). They examined their blood at weekly intervals for four weeks. The CD4 counts in these patients were markedly reduced, with averages beginning below 500 and staying there for the entire 4 week study period. They also found T-cell function to be diminished, especially in patients who did not survive, although there was no significant difference in CD4 counts between those that died and those that survived. The CD8 cells were also reduced in these patients, and although in AIDS CD8 elevations are considered more typical, in advanced AIDS cases the CD8 count can also be markedly reduced. Because of the serious and life-threatening nature of sepsis, these patients would be more similar to advanced AIDS, and so their immune system profile is likely to be similar. The authors did not provide individual CD4 counts, nor do they present data showing how many patients have CD4 counts below 200, but having an average below 500 is still highly significant. Antiretroviral medications would be started at this time if they had been diagnosed HIV-positive, according to the most widely followed guidelines.

2e) Low CD4 counts in pulmonary tuberculosis

Tuberculosis is a relatively common infection in people diagnosed HIV-positive, especially when compared to the general population. It is also relatively common in other people who are immunosuppressed, such as alcoholics, the homeless, intravenous drug users (IVDUs), and people who suffer from malnutrition. In 1985 a group of researchers in Indonesia examined the lymphocyte subsets in 26 patients newly diagnosed with pulmonary tuberculosis (TB) (Beck et al. 1985). They undertook the study because of a previous report of lowered CD4 counts in HIV-positive patients with TB in which the authors assumed that the lowered CD4 counts were due to HIV. They found that in HIV-negative TB patients CD4 counts were also significantly lowered, with an average of 748, compared to 1,043 in healthy controls. Because the CD8 cells were slightly increased, they also found significantly lowered CD4/CD8 ratios. Although the effects seen here were not as dramatic as in the studies reviewed previously, with only 5 of 26 patients having CD4 counts less than 500, the authors still felt their findings were highly significant to people diagnosed HIV-positive. Here are some of their comments:

"In a study of AIDS, ... Vieira et al. stated that it was possible, but highly unlikely, that tuberculosis or its treatment could have altered the relative numbers of circulating lymphocytes bearing the markers CD4 ... and CD8, but they dismissed this possibility because of the severity of the altered CD4/CD8 ratio... We now report the relatively frequent occurence of moderate CD4 lymphopenia in patients with untreated but otherwise uncomplicated pulmonary TB." (Beck et al. 1985, page 50)

The authors also comment on some similar findings in leprosy, as well as in HIV-negative hemophiliacs:

"Moderate reduction in the CD4/CD8 ratio has been reported in lepromatous leprosy, which reverts to normal under effective chemotherapy... It is tempting to speculate that these changes are analogous to those we now report in tuberculosis and that they are a consequence of ongoing immune response to the disease... Interestingly, comparable CD4 lymphopenia has been reported haemophiliacs treated with factor VIII, from a population apparently free from AIDS, and this change has been attributed to a reaction to transfusion of foreign proteins." (Beck et al. 1985, page 53).

The reports of the effects of factor VIII transfusions on CD4 counts have since been confirmed, as will be presented in section 3.

2f) Nearly all viruses interfere with lymphocyte function

In 1987 a summary article appeared in the Annual Review of Immunology entitled simply, "Viruses Perturb Lymphocyte Functions" (McChesney & Oldstone 1987). This article did not look at CD4 counts, but rather focused on the ability of CD4+ T-cells and other cells to proliferate when presented with an antigen. The authors reviewed evidence that a multitude of viruses interfere with the ability of CD4+ T-cells to proliferate. Following are some direct quotes from the text:

"Viruses with every type of genomic nucleic acid, encompassing divergent replication strategies, are now known to infect lymphocytes. The list (Table 1) of viruses that infect lymphocytes is not comprehensive, but rather indicates representative viruses from different taxonomic groups. With few exceptions, immunologic dysfunction has been associated with the infections." (McChesney & Oldstone 1987, pages 280-281)

The viruses listed in Table 1, that infect human lymphocytes, are: Hapatitis B virus, Group C adenoviruses, Herpes simplex viruses, Cytomegalovirus, measles, mumps, respiratory syncytial virus (RSV), Vesicular stomatitis virus, Inflenza A, Parainfluenza, Rubella, Poliovirus, Lymphocytic choriomeningitis virus, and Human T-cell leukemia viruses I and II.

After a lengthy section focusing on the measles virus, they go on to discuss the class of viruses to which HIV belongs, retroviruses:

"Retroviruses of murine (mouse), avian (bird), feline (cat), and human origin are immunosuppressive as well as oncogenic in their hosts. The evidence of depressed cellular and humoral immune responses... is independent of the transforming function of the virus... There is no interspecies restriction, i.e. both murine and feline retroviruses can suppress mouse and human lymphocyte proliferation in vitro." (McChesney & Oldstone 1987, page 287)

The authors go on to describe that it is not necessary for the entire retrovirus to be introduced, but only some of its proteins, so that the depressed response is apparently a passive one that does not require any action on the part of the viruses being discussed.

"A partially purified 15-kd structural protein of a feline retrovirus inhibited the proliferation of feline lymphocytes... The inhibition was dose dependent and and occured when the protein was added as late as day 3 of a 4-day culture. In contrast, another structural protein, p27, was not inhibitory." (McChesney & Oldstone 1987, page 287)

Unfortunately, at least for the purposes of this paper, the authors do not discuss CD4 cells, specifically.

3) Low CD4 counts caused by injections of foreign proteins

3a) CD4 irregularities in hemophilia

Hemphiliacs were one of the original HIV risk groups. As mentioned above, hemophiliacs who are HIV-negative have been found to have lowered CD4 counts as well as lowered CD4/CD8 ratios, and it appears that this effect is caused by injections of factor VIII. Antonaci et al (1988) for example, found decreased CD4/CD8 ratios as well is impaired CD4 function in HIV-negative hemophiliacs, stating in their conclusion that "Our findings clearly indicate an impairment of immune function in hemophiliacs regardless of HIV infection" (page 318). Similarly, Madhok et al. (1986) found depressed cell-mediated immunity that was independent of HIV status. Their abstract contains the following comments:

"There was no difference in skin response between patients positive and negative for the human immunodeficiency virus (HIV). In the whole group, and in seronegative patients (n = 17), there was an inverse relation between exposure to clotting factor and skin response. In seropositive patients (n = 12) no such association was apparent. This study shows that clotting factor concentrate impairs the cell mediated immune response to a new antigen in the absence of infection with HIV." (Madhok et al. 1986, page 978)
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Old 01-06-2005, 09:58 PM   #35
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3b) CD4 irregularities caused by injected drugs

Intravenous drug users (IVDUs) are another group with a high risk of being diagnosed HIV-positive. In an article published in 1987 in the journal, AIDS, lymphocytes were found to be reduced in HIV-positive injection drug users as a direct function of how many injections they received (Des Jarlais et al. 1987). The authors comment in their abstract:

"Continued drug injection was associated with the rate of CD4 cell loss... While it is not possible to distinguish the mechanism underlying the relationship between continued drug injection and CD4 cell loss, seropositive IV drug users should be warned that continued injections may lead to increased HIV-related immunosuppression." (Des Jarlais et al. 1987, page 105)

A similar finding in 1991, also published in the journal, AIDS, found that lymphocyte reactivity was much more significantly reduced in IVDUs who injected more frequently, regardless of whether or not they were HIV-positive (Mientjes et al. 1991). Although the CD4 cell function was impaired, no difference was found in CD4 counts due to frequent injecting. They did find that HIV-positive IVDUs had lower CD4 counts than did HIV-negative IVDUs, however. The T-cell reactivity was 40-50% lower in IVDUs who were injecting 3 times a day for the preceding several months when compared to a similar group who had not injected in the preceding months, regardless of their HIV status. The authors write: "We conclude that lymphocyte reactivity is depressed by frequent injecting in both HIV-negative and HIV-positive drug users" (Mientjes et al. 1991, page 35).

As far back as 1980, a report in the Journal of Immunology documented lowered T-lymphocytes in IVDUs from Georgia, Illinois, and Massachusetts (McDonough et al. 1980). The authors found that IVDUs in their study had about half to one third as many T-lymphocytes, expressed as a percentage, as control populations. Although they did not look specifically at CD4+ T-lymphocytes, it has been found that when total T-lymphocytes are reduced, CD4 counts are also normally reduced (Kotze 1998). They discuss previous findings of opiate receptor sites on T-lymphocytes, suggesting that the IV opiates were the cause of the lowered T-cells, but they also recognize other possible contributing factors:

"Since most street heroin addiction involves polydrug use including chronic use of marijuana, barbiturates, hallucinogens, and other illicit substances, the hypothesis can be proposed that the depression of T-lymphocyte percentage was caused by another drug or combination of drugs, or by the effect of drug use on the addict's general physical health and nutrition, i.e., the addict milieu." (McDonough et al. 1980, page 2542)

The finding that a wide variety of physical and psychological stressors can lower CD4 counts supports this multifactorial argument, in which general health and nutrition can be significant contributing factors.

Finally, a review paper that was published in 1995 in the journal, Immunopharmacology, had an interesting discussion of the significance of this information for IVDUs diagnosed HIV-positive.

"Among the unwarranted side effects of respiratory depression, constipation, and physical dependence are the immunosuppressive qualities, particularly those which affect cell-mediated immunity. The immunosuppressive characteristics of opioid narcotics (e.g., morphine) have recently come into focus with the advent of acquired immune deficiency syndrome (AIDS) and the putative causative agent, human immunodeficiency virus type 1 (HIV-1). Specifically, a vast reservoir of HIV-1-infected individuals exists among drug abusers. Moreover, experimental evidence would suggest narcotic opioids may increase viral load in infected individuals." (Carr et al 1995, page 59).

3c) CD4 Irregularities caused by in utero exposure to opiates

In 1987, a study found that infants exposed to intravenous drugs in utero also have decreased CD4/CD8 ratios and reduced CD4 function, even when they are HIV-negative (Culver et al 1987).

"The CD4/CD8 ratio decreased with age in the drug-exposed infants compared with control infants (P less than 0.005). ... Our data demonstrate that infants of intravenous drug-using mothers have distinct immunologic differences at birth compared with non-drug-exposed infants and that these persist throughout the first year of life. The cause appears unrelated to intrauterine viral infection, suggesting a direct toxic effect of the drugs on fetal immunologic development." (Culver et al. 1987, page 230)

These results show that multifactorial causes of low CD4 counts probably apply to all age groups, including newborns. This is especially true in the United States and in Europe where most newborns who are HIV-positive are born to women who use intravenous drugs. In Africa, malnutrition and other infectious diseases are more likely to contribute, as will be discussed below.

4) Low CD4 counts caused by injuries and burns

Several studies over the years have looked at the effects of severe injuries or burns on CD4 counts. An early report appeared in 1982, in which the authors looked at the percentage of CD4 counts in 30 patients admitted to their hospital's burn center (Antonacci et al. 1982). They found that the severity of the burns was directly correlated with depressed CD4 percentages. Patients with greater than 25% of their body covered with 3rd degree burns had the lowest percentages on admission, 37%, as compared to normals who had 63%. They found a similar pattern with the CD4/CD8 ratio, but do not report on absolute CD4 counts.

In 1984, a group of researchers decided to look at lymphocyte subsets in patients with multiple trauma who had no burns (O'Mahoney et al. 1984). They examined the blood of 31 patients and compared their lymphocyte profile to ten normal controls. The CD4/CD8 ratio was significantly reduced and inverted, with an average of 0.96, compared with 1.82 in controls. They also found reduced lymphocyte proliferation/blastogenesis in response to antigen challenges. While their original report said they found no difference in absolute CD4 counts, they report in a postscript that they were mistaken in this regard: "in looking back now at the data, we feel the CD4 population did change relative to the CD8 population because of an absolute decrease in the number of CD4 cells" (O'Mahoney et al. 1984, page 875). The CD8 cells were slightly increased, as is also seen in people diagnosed HIV-positive.

In 1985, a study was published by some of the same researchers that looked at two groups of patients with severe injuries, a group of 25 patients with burns, and a group of 21 patients with non-thermal injuries (O'Mahoney et al. 1985). Both groups had severely lowered CD4 percentages, which persisted until 50 days post-injury when the study was concluded. They also found that people with lower CD4 percentages were more likely to develop sepsis. Here are some of the author's comments:

"The most important abnormality appears to be a reduction in CD4 positive cells in burn patients... A change in the ratio of CD4 to CD8 positive cells soon after injury is due to a reduction in CD4 positive cells, not an increase in CD8 positive cells." (O'Mahoney et al. 1985, page 584).

"We believe that the more important abnormality in the patients studied is a reduction in T-cell help - both in terms of the number of circulating CD4 positive cells and a reduction in interleukin 2 production seen both in burn and non-thermal injury patients. Interleukin 2 is produced by T-cells, especially CD4 positive cells, and promotes their growth and stimulates clonal expansion of T-cell subsets: it is thus crucial in the response to foreign antigen." (O'Mahoney et al. 1985, page 585).

The final study to be reviewed is also quite old, from 1986, and looked at 20 consecutive patients who had emergency surgery due to major trauma (Polk et al. 1986). This was the only study of trauma victims where absolute numbers of CD4 cells are given, which makes it more significant from the perspective of this paper. Figure 7 on page 289 shows that 6 of 20 (30%) patients had CD4 counts below 200 cells/mm3, and 13 of 20 (65%) had counts below 500. The authors state simply: "Total T-cells represent what is interpreted as a normal and common response to injury... All patients had low total lymphocyte counts on admission and exhibited a furthur decline on day 3" (Polk et al. 1986, page 287). 10 of the patients also had major infections, and three had minor infections, which may have also contributed to their extremely low CD4 counts. This paper is distinctive in that it attempts to explain a mechanism for the lowered CD4 counts, citing a study supporting the hypothesis that increased cortisol levels are responsible for the decline, and that increased cortisol is also a normal response to injury. They also argue that the reduction in CD4+ lymphocytes probably does not represent cell death, but rather redistribution out of the bloodstream and into the tissues. The argument that cortisol plays a key role in lowered CD4 counts will be encountered again in the section on psychological stress.

5) Low CD4 counts in normal human pregnancy

Several studies have been published on CD4 counts during normal pregnancy. Most recently, Burns et al.published a study in 1996, where they attempted to control for potentially confounding factors like the increased blood volume that normally occurs in pregnancy. They used CD4 percentages because of this variable, and determined that "Our CD4 cell findings for HIV-negative women are consistent with the majority of prior studies, which demonstrate a decline in CD4 levels during normal pregnancy" (Burns et al. 1996, page 1465). They also found that HIV-positive women had a more severe decline which did not correct post-partum as it did in HIV-negative women, although they fail to take into account other factors that can cause lowered CD4 counts. These include any infections that the women may have experienced, the traumatic effects of C-sections which are normally performed on HIV-positive women to prevent neonatal transmission, or the potentially severe psychological stress of worrying if their baby will also be HIV-positive, which can take up to 18 months to determine.

In 1989 a study was published of normal pregnancy which found reduced CD4 percentages in the 1st and 2nd trimester, as well as reduced CD4/CD8 ratios in the 2nd trimester (Castilla et al. 1989). They comment on previous studies looking at a variety of lymphocyte changes during pregnancy, stating simply, "In these studies, variation in the number and proportion of CD4+ lymphocytes is the alteration most frequently reported" (Castilla et al. 1989, page 104). The percentage of CD8+ lymphocytes was unchanged. They also claim that "we have accounted for all the presently known factors that can alter the concentrations of T-cell subsets in blood" (Castilla et al. 1989, page 104), but in fact they did not consider any of the factors described in this paper, such as infections, trauma, overexercising, normal daily variation, or psychological stress. This demonstrates that even clinicians and researchers doing studies that focus specifically on CD4 levels are often unaware of how many different conditions cause low CD4 counts.

The final study to be reviewed here is an early one from 1982 (Sridama et al. 1982). These researchers found reduced absolute CD4 counts, as well as reduced percentages of CD4+ T-cells in 76 women with normal pregnancies. By the third trimester, the pregnant women had an average of only 543 + 169 CD4+ T-cells, compared to 1073 + 441 in non-pregnant women who served as controls. Both the absolute numbers and the percentages stayed low until several months post-partum, and similar results were obtained for the CD4/CD8 ratio which was also reduced. B-cells were increased which is compatible with the increased antibody levels normally found in human pregnancy, and which are also commonly seen in people diagnosed HIV-positive. This is the only study found of normal pregnancy that provides data on absolute CD4 counts, and the average of 543, with a standard deviation of 169, means that a relatively large percentage of these women had levels lower than 500, the point at which antiretroviral medications would be started in someone diagnosed HIV-positive.

6) Reduced CD4 counts from overexercising

Only one study will be discussed in detail here, which was published in 1992 (Verde et al. 1992). In a controlled trial, ten athletes were asked to over-train for three weeks. Blood samples were taken immediately before starting, at the end of the three weeks, and again three weeks after returning to normal. The researchers found steady declines in the percentage of CD4+ T-cells, with the lowest amount occuring 3 weeks after returning to a normal exercise schedule. The authors also found reductions in the CD4/CD8 ratio, although these had normalized by the 3 week endpoint. Finally, the authors also checked levels before and 5 minutes after acute exercise, and again found reductions in CD4 percentages and in CD4/CD8 ratios, although these normalized by 30 minutes post-exercise. It is interesting that a stress as simple as overexercising for three weeks could cause lowered CD4 counts, and that they did not correct for at least three more weeks after returning to a normal exercise schedule.

Other studies have found increased infections in athletes, especially during periods of heavy training or competition, which suggest the presence of "clinically relevant immune suppression in well trained athletes" (Mackinnon 1997).
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Old 01-06-2005, 09:59 PM   #36
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7) Low CD4 counts in malnutrition

A number of studies have looked at the immunosuppression that results from malnutrition. Like the other conditions covered in this paper, malnutrition causes severe immunodeficiency with depletion of CD4+ T-cells and reduction of cell mediated immunity. One of the most recent studies is from India, where malnutrition is extremely common (Hegde et al. 1999). The authors found that reduced CD4 counts were a natural physiological effect of malnutrition, and comment that both HIV and malnutrition lead to a state of anergy with failure of cell-mediated immunity. They also point out that HIV usually occurs in conjunction with several other stressors of the immune system: "micronutrient abnormalities, concomitant infections, and genetic factors are some of the compounding co-factors which furthur contribute to the deterioration of immune functions in AIDS patients" (Hegde et al. 1999, page 318).

A review paper from the Journal of Nutrition in 1996 also compares malnutrition and AIDS, saying that "Protein/energy malnutrition or deficiencies of single nutrients that assist in nucleic acid metabolism generally lead to atrophy of lymphoid tissues and dysfunctions of cell mediated immunity" (Beisel 1996, page 2611S). The author comments on a syndrome of immunosuppression caused by malnutrition which is called "NAIDS", and states that it often occurs in people diagnosed HIV-positive:

"Immunological dysfunctions associated with malnutrition have been termed Nutritionally Acquired Immune Deficiency Syndromes (NAIDS). Infants and small children are at great risk because they possess only immature, inexperienced immune systems and very small protein reserves. The combination of NAIDS and common childhood infections is the leading cause of human mortality. NAIDS can generally be corrected by appropriate nutritional rehabilitation, but from a viewpoint highly important to this Workshop, AIDS and NAIDS are intensely synergistic... Aggressive nutritional support for children with HIV infections could delay, or lessen, the development of NAIDS and avoidance of NAIDS would improve both quality and length of life." (Beisel 1996, page 2611S)

Later in the paper they describe some of the immunological changes and clinical courses often seen in malnutrition, which sound very similar to AIDS.

"Generalized, protein energy malnutrition causes widespread atrophy of lymphoid tissues, especially in children. The thymus, spleen, tonsils, and lymph nodes are all affected, with evidence of atrophy being greatest in T-lymphocyte areas of these tissues. ...

Malnutrition, in turn, leads to a variety of immune system dysfunctions, ... which allow infectious diseases to fluorish. These closely linked events can initiate a "downhill spiral" or a "vicious cycle" that leads inexorably to death."

"Protein energy malnutrition causes a marked repression of cell-mediated immunity and the function of T-lymphocytes. Malnourished children show anergy with loss of delayed dermal hypersensitivity reactions and a decrease or reversal of the CD4/CD8 cell ratio... In contrast, B-lymphocyte numbers and functions appear to be maintained. While existing antibody production is conserved or even increased during malnutrition, antibody responses and antibody affinity are impaired." (Beisel 1996, page 2612S)

The "downhill spiral" of opportunistic infections that "lead inexorably to death" is particularly reminiscent of a description of AIDS. Beisel also reviews similar effects of deficiencies of specific nutrients, such as vitamin A and zinc:

"Deficiencies of single essential nutrients with important roles in nucleic acid synthesis and metabolism appear to cause derangements in immunological functions that are quite similar to those seen in protein energy malnutrition ... Both vitamin A and zinc deficiencies are characterized by lymphoid tissue atrophy and depressed cellular immunity..." (Beisel 1996, page 2613S)

To provide an idea of how prevalent the problem of malnutrition is worldwide, he points out that the combination of malnutrition induced immunosuppression and childhood infections "is the leading cause of human mortality, producing more than 10 million deaths per year (i.e. over 25,000 deaths per day)" (Beisel 1996, page 2614S).

Another review paper published one year later, in 1997, made similar arguments about the significance of malnutrition in impairing immunity (Chandra 1997). This is the only paper found

that gives percentages of CD4 cells, although absolute CD4 counts are still not provided. Figure 3 on page 462S shows that the percentage of CD4+ T-cells in normal well-nourished children is about 45%, while the percentage in malnourished children is only 25%. Chandra describes the immune system changes seen in malnutrition:

"Nutrition is a critical determinant of immune responses and malnutrition the most common cause of immunodeficiency worldwide. Work done in the past 25 years has confirmed that impaired immunity is a critical adjunct factor in malnutrition-associated infections. ... Lymphoid atrophy is a dramatic feature of protein energy malnutrition. ... Delayed hypersensitivity cutaneous responses are markedly depressed. It is not uncommon to have complete anergy to a battery of different antigens. These changes are observed in moderate deficiencies as well. The skin reactions are restored after appropriate nutritional therapy for weeks or months. ... the proportion of helper T-lymphocytes (CD4+ T-cells) is markedly decreased, and the ratio of CD4 to CD8 cells is significantly lower than in well-nourished control subjects." (Chandra 1997, page 460S-461S)

From this review it is seen that not only are the CD4 percentages markedly reduced (from 45% to 25%), but that it takes "weeks or months" of nutritional therapy for the effects of malnourishment to revert to normal.

The final article to be examined is also a review (Harbige 1996). This paper mentions similar findings to the ones already discussed, including lowered CD4+ lymphocytes, decreased T-cell function, and anergy. It also mentions the increase in antibody levels which is also seen in people diagnosed HIV-positive, specifically serum IgG, IgM, IgA, and IgD. In contrast to serum IgA, however, secretory IgA is diminished. The main addition that this paper provides which others did not is the mention of specific infections that are particularly common in people who are malnourished:

"Among the many infectious organisms commonly associated with protein energy malnutrition are Paramyxovirus (Measles), Rotaviruses, Mycobacterium tuberculosis, E-coli, Shigella, E-histolytica, and Pneumocystis carinii." (Harbige 1996, page 289)

Two of these organisms, M. tuberculosis and Pneumocyctis Carinii, result in the diagnosis of AIDS when they occur in someone who has already been diagnosed HIV-positive. Pneumocystis carinii pneumonia, or "PCP", is perhaps the single infection most commonly associated with AIDS in the United States and Europe, while tuberculosis has always been very common in Africa, and is today considered by some to be a common "AIDS defining" illness there.

This information concerning malnutrition-induced immunodeficiency and opportunistic infections is obviously significant for Africa, where malnourishement is common and where HIV is also thought to be the most prevalent, but it also may be very significant for people in the United States and Europe. Several articles point to malnourishment as a very common problem in AIDS due to decreased nutrient intake or malabsorption (Babameto & Kotler 1997, Keusch & Thea 1993). These problems with nutrient intake can be caused by infections of the oral cavity and gastrointestinal tract, which are quite common in people diagnosed with AIDS. Antiretroviral medications, which cause diarrhea and/or vomiting in well over half of the people who take them, also have the potential to interfere significantly with nutrient intake. In addition, decreased appetite is one of the standard symptoms of depression, which is common in people diagnosed HIV-positive. Many years ago a "giving-in-giving-up" complex was described that can result in people becoming ill and dying before their disease has progressed. A disease like AIDS, with the hopeless description provided to people diagnosed HIV-positive together with the the social stigma that accompanies it, could be particularly susceptible to this phenomenon (Engle 1968). Here are some quotes from a review that focuses on malnutrition in HIV and AIDS, which was published in Gastroenterology Clinics of North America in 1997:

"Malnutrition is a common complication of HIV infection and plays a significant and independent role in its morbidity and mortality. Malnutrition was one of the earliest complications of AIDS to be recognized, and unexplained weight loss i one of the most common initial AIDS defining diagnoses to be given to people who were previously diagnosed HIV-positive..."

"The development of malnutrition in clinical disease generally is believed to be secondary to the underlying disease, and improvement is believed possible only by addressing the underlying disease. Studies have shown, however, that the effects of malnutrition in HIV/AIDS are independent of immune dysfunction per se..."

"Malnutrition associated with HIV infection has far reaching ramifications... Many patients become too debilitated to work steadily and come to rely on public or other assistance. Weight loss is often the initiating event in a vicious cycle of increased fatigue and decreased physical activity, including the ability to prepare and consume food." (Babameto & Kotler 1997, pages 393-394)

The authors do not comment on the emotional burden of HIV/AIDS or how this burden may reduce the person's appetite significantly, which could add strength to the "vicious cycle" described above. Finally, infections of any type put a physical stress on the system which results in loss of weight (Scrimshaw & SanGiovanni 1997). This is because people break down their own tissues to use as fuel, resulting in increased nutrient requirements. A review article that examined this issue states:

"Infections, no matter how mild, have adverse effects on nutritional status. The significance of these effects depends on the previous nutritional status of the individual, the nature and duration of the infection, and the diet during the recovery period [all of these factors are often adversely affected in people diagnosed HIV-positive]. Conversely, almost any nutrient deficiency, if sufficiently severe, will impair resistance to infection." (Scrimshaw & SanGiovanni 1997)

Based on the articles examined above, it could easily be argued that food, social support, and financial independence are solutions that should be given a much higher priority when offering aid to poorer nations. They also suggest that food, financial independence, and social support should be a much higher priority for HIV and AIDS programs in wealthy nations, as well.

8) Daily variation of CD4 counts

Only one study concerning the daily, or diurnal, variation in CD4 counts will be reviewed here (Malone et al. 1990). The authors compared the diurnal variation in HIV-positive and HIV-negative people, finding a significant variance in both. They found that greater variations occurred in HIV-negative people, but that both groups followed a pattern that coincides with known daily fluctuations of cortisol, with minimum CD4 levels occuring between 8:00 and 10:00 a.m., and maximums occuring at around 10:00 p.m.. Cortisol has a daily variation with maximums at about 8:00 a.m., and, as will be reviewed later in this paper, cortisol also causes low CD4 and total T-lymphocyte counts. People with lower baseline CD4 counts had much less diurnal variation. A flattening of the normal diurnal variation of cortisol, together with elevated average cortisol levels, is often seen in people under chronic psychological stress, and is also common in people diagnosed HIV positive. Babameto & Kotler (1997) state simply "Endocrine alterations in HIV infection include elevations in serum cortisol and loss of the normal diurnal periodicity" (page 401). They do not comment on the causes of these altered cortisol levels but chronic psychological stress is a possibility given the stress associated with being diagnosed HIV-positive or diagnosed with AIDS. Malone et al.'s study of CD4 variation found that HIV-negative people had an average variation of 506 cells/mm3 each day, while HIV-positive people had only about 60 cells/mm3 of variation. The authors caution that even this blunted variation is significant, however, stating "3 of 12 HIV-positive patients had CD4+ cell counts below 200 cells/mm3 in the morning but had greater than 200 cells/mm3 in the afternoon" (Malone et al. 1990, page 150). In other words, in the morning they would be diagnosed with AIDS, but if their blood was checked in the afternoon they would just be HIV-positive, albeit with a relatively low CD4 count. They found similar results for total lymphocyte counts, but CD4/CD8 ratios did not have statistically significant changes. The authors conclude that blood draws for CD4 counts should always be done at the same time of day, but they do not comment on relations between the diurnal cycle they observed and the diurnal variation in cortisol.

9) Changes in CD4 counts and lymphocyte function due to psychological stress and social isolation

A large number of studies have looked at the effects of stress on the immune system, and several reviews have been published on this topic (Bonneau 1993, Castle 1995, Herbert 1993, Kennedy 1988, Kiecolt-Glaser 1984, 1991, 1992 Laudenslager 1983, Pariante 1997, Stefanski 1998). These studies have looked at people under chronic stress, such as people suffering from depression, people who were recently divorced or separated, college students during exams, and people who are the primary caregivers of demented family members. There are also a number of studies of animals under stress. Stress causes a state of immunodeficiency characterized by a reduction of the number of T-lymphocytes, with special targeting of CD4, helper T cells. There is also a reduced CD4/CD8 ratio, with a relative increase in CD8, suppressor/cytotoxic T cells. Unfortunately for the purposes of this paper, the vast majority of studies look at lymphocyte function and total T-cell counts. The few studies that have looked at CD4 cells used percentages (Kiecolt-Glaser et al. 1992).

A group of researchers led by Robert Sapolsky has done a great deal of work observing the effects of psychological and social stress on baboons and other primates, with most of their work focusing on the neurotoxicity that is caused by stress, with dementia and loss of neurons in the hippocampus (Sapolsky 1990, 1996). In one study, however, they measured total lymphocyte counts and cortisol levels in a group of baboons that were invaded by a highly aggressive young male baboon, whom they named Hobbs (Alberts et al. 1992). Hobbs was particularly threatening to females in the group, and was apparently attempting to use fear, physical intimidation, and abuse to increase his chances of successful mating. Cortisol levels in the group nearly doubled after Hobbs joined the group, with a slightly greater increase among females. T-lymphocytes plummeted in the group, from a pre-Hobbs level of 67 per 10,000 red blood cells to a level of about 39, a drop of 42%. When looking at only the levels in baboons who were victims of Hobbs' aggression, the levels fell even more steeply, to only 29 per 10,000 RBC's, a drop of 55%. Interestingly, Hobbs, himself had the lowest number of lymphocytes in the entire group, and the highest cortisol level, suggesting that his behavior may have been taking an even greater toll on his system than it did on the victims of his aggression. Field conditions prevented them from determining the number of lymphocytes per microliter of blood, or from specifically measuring CD4 cells, and the authors comment on their use of lymphocyte counts instead of more sophisticated methods:

"Whereas most studies of the effects of stress upon immunity examine functional indices of immune competence (e.g. mitogen stimulation tests, antibody generation, cytokine responsiveness), our field conditions limited us to this rather crude quantitative measure of numbers of cells." (Alberts 1992 page 174)

It is interesting that these researchers consider T-cell counting to be a crude measure of immune competency. Although the clinicians in this study could not report on CD4 counts, low total lymphocyte counts are associated with low CD4 counts (Kotze 1998), so the findings of this study are likely to indicate that CD4 counts are also lowered..

A review from as far back as 1988 also examined how the immune system was affected by stress, with the following comments regarding CD4 helper T-cells (Kennedy et al. 1988):

"Data are given which document immunosuppressive effects of commonplace, short-term stressors, as well as more prolonged stressors, such as marital disruption and caregiving for a relative with Alzheimer's disease. Immune changes included both quantitative and qualitative changes in immune cells, including changes in herpes virus latency, decreases in the percentages of T-helper lymphocytes and decreases in the numbers and function of natural killer cells. These effects occurred independently of changes in nutrition. Psychological variables, including loneliness, attachment and depression were related to the immune changes. The data are discussed in a framework in which quality interpersonal relationships may serve to attenuate the adverse immunological changes associated with psychological distress, and may have consequences for disease susceptibility and health." (Kennedy et al. 1988, page 77).

Another review, published in 1993, performed a meta-analysis of all studies that looked at psychological stress and the immune system (Herbert & Cohen 1993). In their discussion they mention their findings regarding CD4, helper T-cells:

"In terms of cell numbers, stress is reliably associated with a ... lower number of circulating B cells, helper cells, cytotoxic cells, and large granular lymphocytes. Stress is also reliably associated with a lower percent of lymphocytes that are T cells, helper T cells, and cytotoxic T-cells." (Herbert & Cohen 1993, page 373)

The last review to be discussed here looked at short-term stressor effects and made similar comments to the two reviews above, again focusing on CD4 percentages instead of absolute CD4 counts:

"The immunological changes observed following short-term stressors are very similar to those that have been described following epinephrine injections: increased percentages of natural killer cells, decreased blastogenesis in response to mitogens (decreased lymphocyte function), and decreased percentages of CD4 cells. Total T cells and monocytes did not change." (Kiecolt-Glaser et al. 1992, page 680)

This quote mentions epinephrine injections, but cortisol injections also produce similar effects on the immune system. Secretion of these hormones is the most commonly proposed mechanism for the immunosuppression that occurs during states of acute or chronic psychological stress. One of the major changes during times of stress is an outpouring of the hormones epinephrine and cortisol, which lead to a dramatic reduction in the number of T-lymphocytes. The strength of the correlation between decrease in T-cells and excess cortisol is so strong that low T-cells is one of the diagnostic criteria for identifying excess cortisol. Here are some quotes on this topic from a basic textbook of physiology (Guyton 1996).

"Almost any type of physical or mental stress can lead within minutes to greatly enhanced secretion of ACTH and consequently cortisol as well, often increasing cortisol secretion as much as 20-fold." (Guyton 1996, p.966).

"Cortisol suppresses the immune system, causing lymphocyte production to decrease markedly. The T lymphocytes are especially suppressed." (Guyton 1996, p.964)

"Cortisol decreases the number of eosinophils and lymphocytes in the blood; this effect begins within a few minutes of injection of cortisol and becomes marked within a few hours. Indeed, a finding of lymphocytopenia or eosinopenia is an important diagnostic criterion for overproduction of cortisol by the adrenal gland. Likewise, the administration of large doses of cortisol causes significant atrophy of all the lymphoid tissue throughout the body... This occasionally can lead to fulminating infection and death from diseases that would otherwise not be lethal, such as fulminating tuberculosis in a person whose disease had previously been arrested." (Guyton 1996, p.965).

It is interesting that this description of 'fulminating infection and death from diseases that would otherwise not be lethal' sounds very similar to a description of AIDS. Cecil's Textbook of Medicine also discusses the specific lowering of CD4 counts that corticosteroids cause:

"A significant T lymphocytopenia occurs with a selective egress from the circulation of CD4+ "helper-inducer" T cells, whereas CD8+ "cytotoxic-suppressor" T cells are relatively resistant to these effects (see Chapter 270). B lymphocytes are less susceptible to glucocorticosteroid-induced effects than T cells, with little alteration in intravascular number or composition... A variety of lymphocyte functions, including activation, proliferation, and differentiation, are sensitive to glucocorticosteroids. Although glucocorticosteroids do not affect T-cell activation, down-regulation of RNA synthesis decreases proliferation... Unlike T cells, B-lymphocyte function is only modestly affected by glucocorticosteroids. Within 1 month of glucocorticosteroid therapy, reduction in serum immunoglobulins is noted because of increased catabolism. Antibody responses to injected antigens are not impaired." (Goldman 2000, page 111)

This sounds exactly like what is described in AIDS, with selective lowering of CD4 counts, normal or increased CD8 counts, and normal or increased antibody titers in the early stages. The similarity is so striking that one cannot help but wonder if factors that increase cortisol, such as chronic and severe psychological stress, could be major players in the immunosuppression observed in AIDS. What is even more curious, however, is that cortisol analogues are often used in people diagnosed with AIDS to treat conditions such as pneumocystis carinii pneumonia, a topic that will be discussed in the next section, entitled "Immunosuppression caused by drugs used in the treatment of people diagnosed HIV-positive".

There is a disease which is characterized by long-term hypersecretion of cortisol, called Cushing's syndrome or Cushing's disease. Cecil Essentials of Medicine describes the physical manifestations of Cushing's disease, many of which are also common in AIDS:

"Regardless of the etiology, hypercorticolism results in central obesity, carbohydrate intolerance, muscle wasting, and osteoporosis. Obesity is centripetal, manifested typically by a "buffalo hump", increased supraclavicular fat pads, and moon facies... Depression occurs often, and, rarely, patients may be frankly psychotic." (Andreoli et al. 1993)
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Old 01-06-2005, 10:00 PM   #37
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Muscle wasting, depression, and dementia-associated psychosis are all relatively common findings in people diagnosed with AIDS. Cushing's disease also causes immunodeficiency (Britton et al. 1975) and dementia with loss of cortical neurons (Starkman et al. 1992), both of which are characteristic of people diagnosed with AIDS. It is also interesting that the redistribution of fat described here is a common side effect seen in HIV-positive patients after long-term protease inhibitor use, with the same "buffalo hump" and central obesity, which has been referred to as a "protease paunch". Early osteoporosis has also been recently found to be another common adverse effect of these medications.

Multiple studies have found that people diagnosed HIV positive have chronically elevated cortisol levels, suggesting that the low CD4 T-cells in people diagnosed with AIDS could be at least partly caused by elevated cortisol (Azar 1993, Christeff 1988, 1992, Coodley 1994, Lewi 1995, Lortholary 1996, Membreno 1987, Norbiato 1996, Norbiato 1997, Verges 1989). It is important to note, however, that chronic stress can induce immune suppression even when cortisol and epinephrine are not elevated (Bonneau 1993, Keller 1983), so that the mechanisms by which stress affects health and immunity are not completely understood.

In 1998, a group of researchers put the stress-cortisol hypothesis to the test by checking CD4 counts and cortisol levels in people who were randomly assigned either to a bereavement support group intervention or to a wait-list control (Goodkin et al. 1998). The intervention consisted of 10 weekly support group meetings, and blood samples continued to be taken periodically for a total of 6 months. Some of the group members were HIV-positive, and the authors stratified their data according to HIV status. They found that CD4 counts were increased in people receiving the support group intervention as compared to controls, and that these increases correlated with reduced levels of the stress hormone cortisol. Here is their description of the results:

"In HIV-negative intervention subjects, the CD4 cell count increased 112 cells/mm3, while that in HIV-negative control subjects decreased 88 cells/mm3, for a difference of 200 cells/mm3 between treatment and control groups. In treated HIV-positive individuals, the CD4 cell count was stable, within laboratory error over the entire six months. However, that in HIV-positive controls decreased 61 cells/mm3. Both (statistical tests) demonstrated a statistically significant intervention effect on the CD4 cell count." (Goodkin et al. 1998, page 387)

Results like these may help to explain why socially isolated people, when compared to people with high levels of social support, have been found in over eight studies to have between double and triple the death rates from all causes (Berkman 1979, House 1988, Ornish 1997). A recent study found that people diagnosed HIV positive were two to three times more likely to 'progress to AIDS' if they were socially isolated and under high levels of stress (Leserman et al. 1999). Here is a brief quote from the abstract of their paper:

"Faster progression to AIDS was associated with more cumulative stressful life events (p<0.002), more cumulative depressive symptoms (p<0.008), and less cumulative social support (p<0.0002)... At 5.5 years, the probability of getting AIDS was about two to three times as high on those above the median on stress or below the median on social support..." (Leserman et al., page 397)

This study was not able to assess the impact of the stress of living with the diagnosis, HIV-positive, nor can any study that is ethically designed. It is not unreasonable, however, to infer that the stress of the diagnosis is a strong contributor to immunosuppression in people diagnosed HIV-positive, and even a contributor to mortality.

In addition to the cortisol hypothesis, another mechanism has been presented in a paper in the journal, Medical Hypothesis (Shallenberger 1998). The author presents a multifactorial model of AIDS in which the immune system becomes overbalanced towards antibody-mediated immunity (AMI) when it is chronically stressed. He does not feel that HIV is necessary to create this imbalance, and cites similar evidence to what has been cited here. When AMI becomes dominant, the cytokines released by this arm of the immune system (interleukins 4 and 10) naturally suppress the other arm, called cell-mediated immunity (CMI). CMI uses CD4+ cells in abundance, and when it is suppressed the CD4 count will drop. If the AMI dominance is maintained long enough it can become pathological and be very difficult to reverse, eventually leading to failure of both AMI and CMI, according to Shallenberger. His arguments are supported by the fact that people who are diagnosed HIV-positive invariably have high levels of antibodies, even when their CD4 counts have dropped significantly. Shallenberger carefully documents that evidence of this phenomenon occurs in all the risk groups for HIV, whether or not they are HIV positive, including hemophiliacs, male homosexuals, IVDUs, and transfusion recipients. This AMI dominance mechanism could still be mediated, at least in part, by excess cortisol secretion, but the author does not discuss the cortisol hypothesis in his paper.

10) Immunosuppression caused by drugs used in the treatment of people diagnosed HIV-positive

Many drugs regularly used to treat people diagnosed HIV-positive have severe immunosuppressive effects, as well as other serious adverse effects. These include corticosteroids, AZT, other drugs in the same class as AZT, certain antibiotics, and protease inhibitors. People diagnosed HIV-positive take these drugs indefinitely, which increases the risks of adverse effects significantly.

Corticosteroids, as described above, cause an immunosuppression that is extremely similar to the immunosuppression that is claimed to be caused by HIV, with lowered CD4 counts and sparing of CD8 cells as well as sparing of antibody production. In spite of this, corticosteroids are commonly used in people diagnosed HIV-positive to treat conditions like pneumocystis carinii pneumonia, as the following quote from Cecil's Textbook of Medicine demonstrates:

"The major breakthrough in the search for more effective therapies for Pneumocystis has been the irrefutable evidence that mortality for severe episodes can be reduced nearly twofold by use of corticosteroids within 72 hours after beginning specific anti-Pneumocystis therapy." (Goldman 2000, page 1882)

Thus corticosteroids have been found to reduce mortality from what is perhaps the most common serious infection in people diagnosed with AIDS, and at the same time they cause the exact same immunosuppression that is supposedly allowing pneumocystis to flourish. This seeming contradiction is very difficult to explain, at least if it is true that low CD4 counts are truly the primary problem in people diagnosed HIV positive.

Other medications used to treat people diagnosed HIV-positive, such as AZT and protease inhibitors, also have immunosuppressive effects. AZT, also called Retrovir or zidovudine, continues to be the most commonly used drug in people diagnosed HIV-positive. Up until 1996 it was used alone as a monotherapy, and it was given at a dose that is about triple the dose used today. In 1996 it began to be used in combination with other drugs such as protease inhibitors, and the dose was reduced significantly. Many other drugs that are often used in combination with AZT use the same basic mechanism as AZT and have similar toxicities, including ddI, ddC, 3TC and d4T. The most severe effect of AZT is a lowering of the number of neutrophils, which are the most numerous cells of the immune system, as well as lowering eosinophils, basophils, red blood cells, and platelets. The elimination of neutrophils, eosinophils, and basophils, which are all critically important cells of the immune sytem, is called "granulocytopenia". If the number of neutrophils is lowered, this is called "neutropenia". If someone suffers from granulocytopenia, they also by definition suffer from neutropenia. Neutropenia and granulocytopenia are also common complications of cancer chemotherapy. The clinical course of severe neutropenia, as described in the basic pathology textbook, Pathologic Basis of Disease (Robbins et al. 1994), describes what happens to people with severe neutropenia.

"CLINICAL COURSE: The symptoms and signs of neutropenias are those of bacterial infections. ... In severe agranulocytosis with virtual absence of neutrophils, these infections may become so overwhelming as to cause death within a few days." (p.631).

This sounds quite similar to a description of AIDS. Later stages of HIV infection are often associated with neutropenia as well as low CD4 counts. This may be why many of the AIDS defining diseases are bacterial infections, which are not considered typical infections in people suffering from low CD4 counts and a specific loss of cell-mediated immunity. Robbins (1994) uses italics to highlight the following statement about neutropenia: "the most severe forms of neutropenias are produced by drugs" (Robbins et al 1994, page 630). This is especially true when the drugs are given for long periods, as is true in people diagnosed HIV-positive.

While AZT and other drugs used in combination therapy do not cause low CD4 counts in the short term, it is probable that long term use will also lower CD4 counts significantly, especially if it is given for long periods. This finding has been ignored because the original study of AZT's toxicity to CD4 lymphocytes claimed that very high concentrations, much higher than concentrations used in clinical practice, were needed before CD4+ lymphocytes were affected. What is not mentioned in the Physician's Desk Reference is that AZT has been found in five studies performed afterwards to be equally toxic to CD4+ T lymphocytes. These later studies found that AZT was toxic to CD4 lymphocytes at about the same dosage that is given to people diagnosed HIV-positive (Duesberg 1992).

Glaxo Wellcome puts the following warning in bold-faced, capital letters at the start of the section in the 1999 Physician's Desk Reference that describes AZT.


An earlier version of the Physician's Desk Reference, published in 1992 made the connection even clearer:

"It is often difficult to distinguish adverse events possibly associated with Zidovudine administration from underlying signs of HIV disease or intercurrent illness." (PDR 1992)

Another strongly worded warning appears in the 1996 edition of the United States Pharmacopeia's USP DI: Drug Information for the Health Care Professional .

Because of the complexity of this disease state, it is often difficult to differentiate between the manifestations of HIV infection [sic] and the manifestations of zidovudine (AZT). In addition, very little placebo controlled data is available to assess this difference. (United States 1996, pages 3032-3034)

Granulocytopenia means a deficiency of the most numerous cells of our immune system, which in turn leads to opportunistic infections that can become "so overwhelming as to cause death within a few days" (Robbins et al 1994, page 631). Thus, AZT, by its maker's own admission, can attack a person's own immune system, which is the very thing that HIV is supposedly attacking.

In an article in the journal, Nature Medicine in 1998, the author argues that the initial rise in CD4 count after starting on antiretroviral medications does not represent any decreased killing of CD4+ T lymphocytes, but rather represents shifting of available cells out of the tissues and into the bloodstream (Roederer 1998). The increased T-cell count created by the use of AZT was shown to have no bearing on survival in the best and most well-controlled study available on AZT, the Concorde Study (1994). The Concorde study, which was originally published in the New England Journal of Medicine in 1992, found that people who were given AZT earlier died faster even thought their CD4 counts were higher, although the difference in death rates were not statistically significant (Henderson et al. 1992). Recent evidence shows that AZT and several protease inibitors specifically inhibit microbes that commonly cause infections in people diagnopsed HIV-positive. Protease inhibitors, for example, inhibit Pneumocystis carinii and Candida albicans, two of the most common infections found in people diagnosed HIV-positive (Cassone 1999, Atzori 2000). AZT inhibits many different strains of bacteria, including Enterobacter, Shigella, Salmonella, Klebsiella, Citrobacter, and E-coli, and AZT also acts synergistically with commonly used antibiotics such as Bactrim (PDR 1999). Unfortunately, the antimicrobial effects may be short lived as the following statement indicates: "Limited data suggests that bacterial resistance to zidovudine (AZT) develops rapidly" (PDR 1996, page 1158). It is possible that these drugs may inhibit many other microbes as well, but studies looking at their effects on most microbes have not been done. The finding that they attack microbes may explain the rises in CD4 counts that people on these drugs experience in the short term, since infections with these microbes are associated with extremely low CD4 counts even in the absence of HIV infection. As bacterial resistance develops in the microbes and they again fluorish, however, the CD4 count would naturally begin to fall. It is also possible that the immunosuppressive effects of long-term administration of anti-HIV medications could bring the CD4 count down along with the other white cells.

An example of a study that documented the toxic effects that AZT has on healthy people's immune systems was published in the Annals of Hematology in 1994 (Schmitz et al. 1994). AZT was given to 14 health care workers who had been exposed to HIV-contaminated blood through needle sticks and similar accidents. This type of study is important because the toxicity observed cannot be blamed on HIV, as is quite likely to happen in people diagnosed HIV-positive. None of the 14 workers actually became HIV-positive as a result of their needle stick, which is not surprising since the likelihood of contracting HIV is estimated at about 1 in 333, which is even less than the probablity of finding someone who is HIV-positive when randomly picking from the general population. Fully half of the 14 workers had to quit the drug because of severe toxic effects, and the study was stopped early because of these effects. Only 11 of the 14 people could continue to take the drug for more than four weeks. Neutropenia developed in 36% (4 of 11) of the people who completed 4 weeks of AZT treatment. The three people who could not make it to four weeks dropped out due to "severe subjective symptoms". What is truly remarkable in this study is that these side effects developed in only 4 weeks, while patients diagnosed HIV-positive often stay on AZT and other similar drugs for years.

Other drugs commonly used with people diagnosed HIV-positive have similar immunosuppressive effects. Didanosine (ddI or Videx), is listed in the Physician's Desk Reference (1999) as causing granulocytopenia in 25% of children who had normal values to begin with, and in 62% of children whose values were already abnormal. In adults, 8% experienced "serious" levels of granulocytopenia, compared to 15-19% in patients treated with AZT. Perhaps more significantly, between 13% and 16% experienced serious levels of "leukopenia", which involves reductions of all white blood cells including lymphocytes. The most serious adverse effects of didanosine, as well as lamivudine (3TC or Epivir), stavudine (d4T or Zerit), and zalcitabine (ddC or Hivid), which are all in the same class of drugs as AZT, however, are dose dependent peripheral neuropathy and pancreatitis. Although these effects are unlikely to be blamed on HIV, pancreatitis is a life threatening condition. In Phase 1 trials of didanosine pancreatitis occurred in 9% of people given doses in the range curently used, and it occurred in 27% of people given higher doses. Peripheral neuropathy was even more common, occuring in 51% of people on the higher dose and 34% of people in the dose range commonly used today.

Finally, the drug used to treat and prevent CMV retinitis, gancyclovir, has serious immunosuppressive effects, with a similar bold faced warning in the PDR to what was seen in the section on AZT:


According to current treatment guidelines, gancyclovir is supposed to be started in all people diagnosed HIV-positive if their CD4 counts fall below 100, or if they are diagnosed with CMV retinitis. They are supposed to continue weekly injections of gancyclovir indefinitely, until they die.

An article in the New England Journal of Medicine looked at the muscle wasting, or myopathy, which is caused by AZT, and compared it to muscle wasting that has been presumed to be caused by HIV (Dalakas et al. 1994). Their comments in the abstract indicate a major problem:

"We conclude that long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy, which... is indistinguishable from the myopathy associated with primary HIV infection..." (Dalakas et al 1994, page 1098).

Robbin's text on pathology also contains sections on mitochondrial myopathy, stating that this kind of muscle wasting results in severe weakness. Because it is also associated with neurological symptoms such as dementia, according to Robbins, mitochondrial myopathies "may also be classified as mitochondrial encephalomyopathies" (Robbins et al. 1994, page 1290). Encephalomyopathy, in lay language, means widespread damage to the brain and spinal cord.

Although most retrospective studies have not found AZT to be associated with "HIV dementia, retrospective studies are uncontrolled and thus open to many confounding variables and biases. One of the better controlled studies did find that "HIV dementia" was twice as likely to happen in people taking AZT. In this study, published in the journal Neurology (Bacellar et al 1994), the authors state:

Among subjects with CD4+ cell counts < 200/mm3, the risk of developing HIV dementia among those reporting any antiretroviral use (AZT, ddI, ddC, or d4T) was 97% higher than among those not using this antiretroviral therapy. (page 1895)

Because the authors include only people with low CD4 counts in their comparison, it is less likely that people took AZT because they were already sick. They go on to discuss peripheral neuropathy, which is a degeneration of sensory nerves:

In addition, the findings of our analysis seem to confirm previous observation of a neurotoxic effect of antiretroviral agents. Numerous studies have linked the use of ddI, ddC, and d4T to the development of toxic sensory neuropathies, usually in a dose-response fashion. (page 1895).

These studies are but a sample of the evidence that suggest that AZT and other anti-HIV drugs used as monotherapy or as parts of protease inhibitor cocktail regimens are causing a variety of AIDS-like symptoms which are being blamed on HIV.

11) Unexplained low CD4 counts and "Idiopathic CD4 T Lymphopenia"

In 1992 the Centers for Disease Control (CDC) in Atlanta introduced a new condition characterized by unexplained low CD4 counts in the absence of HIV infection. They called this syndrome "idiopathic CD4 T lymphopenia" (ITL). Bird (1996) provides an excellent summary of this condition, which he calls "Non-HIV AIDS" or "Non-HIV associated immunodeficiency". He concludes that it is distinct from HIV associated immunodeficiency, but he overlooks a number of key points. Several of these points will be reviewed in detail.

Although Bird (1996) does consider the effects of infections on CD4 counts, he fails to take into account most of the conditions reviewed in this paper, such as malnutrition, trauma, burns, intravenous injections of foreign proteins, over-exercising, pregnancy, coricosteroid use, normal daily variation, psychological stress, and social isolation. He also fails to point out that infections alone could easily explain the low CD4 counts found in people diagnosed HIV-positive, who often experience chronic or recurring infections of various types. In addition, malnutrition, injections of foreign proteins, and chronic severe psychological stress are all common in people diagnosed HIV-positive.

It appears that one of Bird's major purposes in writing his paper was to refute the positions of several researchers who question the significance of HIV in causing AIDS. These arguments were being reinvigorated by the discovery of people with low CD4 counts who were HIV negative. Following are the primary positions which Bird attempts to refute:

"1) AIDS is multifactorial with multiple causes. This has been argued by many clinicians and researchers such as Joseph Sonnabend, who has been working with people diagnosed HIV-positive since before HIV was first claimed to cause AIDS." (Sonnabend 1984).

"2) HIV needs cofactors to become active, a position advocated by the discoverer of HIV, Luc Montaignier, and others." (Grau 1998).

"3) Other factors are the only significant ones, and HIV is an opportunistic virus that does not cause AIDS or immunosuppression of any kind. This stance is maintained by a number of prominent researchers including Peter Duesberg, the retrovirologist who first mapped out the genetic code of retroviruses, and David Rasnick, who holds a number of patents in protease inhibitor research." (Duesberg & Rasnick 1998).

Although Bird's paper is thorough in many ways, he overlooks much of the information presented above, and also contradicts itself several times. In the beginning of his paper, he presents a description of how the occurrence of "non-HIV AIDS" was first discovered and made public:

"The unexpected announcement of the Eighth International AIDS Conference, that the US CDC in Atlanta was investigating a series of reported cases of AIDS in which HIV did not seem to be implicated, rekindled many of these issues. At this conference the possibility was discussed that many AIDS cases might not be caused by HIV." (Bird 1996, pages 171-172)

"The majority of cases classified as non-HIV AIDS or CD4+ lymphopenia have been detected following investigation of clinical signs which suggest cellular immunodeficiency. The patients have presented with a history of severe or recurrent infections with intracellular pathogens or virus-associated malignancies which, even before the description of AIDS, were recognised as being highly suggestive of underlying deficiency of cell-mediated immunity. Indeed, it was this constellation of clinical features ... that clearly identified a new clinical entity of AIDS." (Bird 1996, page 173)

After this comparison which reveals just how similar the two conditions are, he goes on to make a similar admission regarding pneumocystis carinii pneumonia:

"Indeed, pneumocystis carinii was first identified as a pathogen amongst severely malnourished (and thus immunodeficient) populations in continental Europe immediately following the Second World War." (Bird 1996, page 173)

Bird does not mention that malnutrition is characterised by exactly the same type of immunodeficiency seen in AIDS, with low CD4 counts, increased immunoglobulins, and severely depressed cell-mediated immunity. He also does not mention how common malnutrition is in people diagnosed HIV-positive (Babameto & Kotler 1997, Keusch & Thea 1993). After these statements describing the similarities between non-HIV associated immunodeficiency and AIDS, he makes several statements in an attempt to distinguish the two. These will be addressed individually.

He states that "the condition (non-HIV associated immunodeficiency) remains exceptionally rare" (Bird 1996, page 176). Even considering only malnutrition, which has a state of immunodeficiency that is very similar to what is seen in AIDS, this statement appears questionable. As outlined above, malnutrition is the leading cause of immunodeficiency worldwide, can be caused by repeated infections, and is very common in people diagnosed with AIDS regardless of their financial status. Other conditions that are associated with very low CD4 counts, such as sepsis, pneumonia, and mononucleosis, are also quite common. Sepsis causes over 100,000 deaths per year in the United States alone, affects young and old alike, and is characterized by markedly lowered absolute CD4 counts, as outlined previously.
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Old 01-06-2005, 10:01 PM   #38
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Another statement that attempts to distinguish between non-HIV AIDS and HIV-induced AIDS is that "most non-HIV immunodeficiency cases have normal or low immunoglobulin levels and also have low CD8 counts" (Bird 1996, page 175). Nearly all of the conditions outlined above were characterized by lowered or inverted CD4/CD8 ratios, showing that CD8+ T-cells at the very least are affected much less than CD4 cells. In many of the conditions discussed above, especially infections, CD8+ T-cells are usually either significantly elevated or normal. Bird himself admits this later in his paper:

"Low CD4 counts have been reported as a transient or long-lasting feature of of a number of acute and chronic infectious diseases. However, in most cases the effect is to lower the percentage of CD4+ cells as a result of increased CD8 cells, rather than as a consequence of absolute reduction of CD4 cells." (Bird 1996, page 179)

Here he not only admits that CD8 cells are often elevated in a wide variety of common human infections, but also makes another serious misstatement regarding CD4 counts. The studies reviewed in this paper clearly show that absolute numbers of CD4+ T-cells are commonly reduced in various human infections, often severely so, in spite of Bird's claim to the contrary. While it is true that CD8 counts were reduced in septic patients, this reduction is often seen in very advanced stages of AIDS, and sepsis is an extremely serious condition which is more comparable to advanced stages of AIDS than it is to earlier stages. Although most studies reviewed did not discuss immunoglobulin/antibody levels, which Bird says are "low or normal" in non-HIV AIDS, malnutrition, which is perhaps the most common condition that occurs in people diagnosed with AIDS, is characterized by increased antibody levels, as described previously. Bird also does not consider that in late stages of AIDS a complete immune collapse is often seen, with lowered CD4, CD8, and immunoglobulin levels, so the use of these parameters to attempt to distinguish non-HIV and HIV acquired immunodeficiency is not particularly reliable.

Bird also states "whereas some cases (of non-HIV associated immunodeficiency) have had a fulminant and fatal outcome, others have been associated with longer term survival associated with stabilisation or reversal of the immunodeficiency" (page 175). Even if a minority of people with non-HIV associated immunodeficiency experience a "fulminant and fatal outcome", however, this is enough to suggest that possible causes of this outcome should be carefully studied. The information obtained from such a study has the potential to provide a great deal of help to people diagnosed HIV-positive, especially considering the studies reviewed above which show how common the conditions associated with low CD4 counts are in this population. Even Bird's stance that "longer term survival" somehow distinguishes them is questionable, however. Long term survival and reversals of CD4 counts are also very common in people diagnosed HIV-positive, although people with progressive downhill courses have received more attention. The average time between a diagnosis of HIV-positive and diagnosis of AIDS is estimated at about ten years, which was based on studies conducted when an opportunistic infection had to be present to diagnose AIDS, i.e. low CD4 counts could not be used for the diagnosis. Between 5 and 15% of people diagnosed HIV-positive never even show immunological abnormalities (Learmont et al. 1992, Ashton et al. 1998, Walton 1999). Finally, at the time of Bird's writing (1996), non-HIV AIDS had only been recently discovered so the potential for a long term outcome could not be determined accurately. Protracted courses with increases and decreases of CD4 counts have always been a common occurrence, even before the introduction of protease inhibitors.

Another statement of Bird's attempts to explain why non-HIV associated immunodeficiency was clustered around AIDS risk groups:

"Although groups at risk of HIV infection appear to be over-represented amongst the early case reports, these almost certainly represent an ascertainment bias... Many of these cases, had they occurred in the general population, might otherwise have escaped detection." (Bird 1996, page 176)

The problem with this line of reasoning is that it also applies equally well to HIV and AIDS, because HIV tests were only routinely given to people in the identified risk groups. It is likely that a very high percentage of people who die of sepsis, multiple trauma, pneumonia, tuberculosis, and malnutrition would qualify for a diagnosis of AIDS based on their clinical and immunologic picture. Indeed, the only obvious difference between them is the result that they have on the HIV antibody tests. Thus a similar ascertainment bias appears to be present in the exclusive focus on HIV. A similar problem exists with Bird's next point regarding non-HIV associated immunodeficiency:

"The other issue that needs to be considered is whether the low CD4 ounts reported in individual patients could be secondary to their particular infections rather than responsible for them." (Bird 1996, page 177)

The problem here is that people diagnosed HIV-positive are even more likely than others to have lowered CD4 counts "secondary to their individual infections", so this is a very poor distinguishing feature. In Bird's own words, as cited previously, "The patients (with non-HIV AIDS) have presented with a history of severe or recurrent infections ... which, even before the description of AIDS, were recognised as being highly suggestive of underlying deficiency of cell-mediated immunity. Indeed, it was this constellation of clinical features ... that clearly identified a new clinical entity of AIDS" (Bird 1996, page 173). In fact the very definition of AIDS, according to the CDC, includes the presence of any one of about 25 different infections in someone who was previously diagnosed HIV-positive (Goldman 2000). Recurrent infections, especially if other conditions such as severe psychological stress are present, could result in a lowered CD4 count that may stay low indefinitely. the fact that Bird overlooks this possibility is even more unusual because he later admits that low CD4 counts can be long-lasting even from a single infection.

"Since CD4 depletion in the blood (after an infection) can persist for long periods, the current CDC definition (of idiopathic CD4 T lymphopenia) is unsatisfactory. I propose that a period of at least 6 months is added to the requirement for consecutive low CD4 counts to rule out short-term secondary effects of infection." (Bird 1996, page 177)

While a six month waiting period would certainly be an improvement, it does not address the possibility that a person could easily suffer another infection within the six month follow-up period, especially if they are prone to recurrent infections. In addition, Bird fails to take into account any of the non-infectious conditions associated with low CD4 counts, which are also quite common. In summary, all of the distinctions Bird attempts to make between non-HIV AIDS and HIV associated AIDS are either weak or nonexistent, which leaves open the possibility that non-HIV AIDS and HIV associated AIDS can be caused by the same factors. Identifying and helping people overcome these non-HIV factors could be more effective than the current practice which focuses solely on trying to eliminate HIV.

Bird also introduces another aspect of CD4 counting which may explain why people initially believed that the low CD4 counts found in people diagnosed HIV positive were a new and unique entity. He points out that the tests that are used to measure CD4 counts were developed at about the same time as AIDS cases were first being identified. This meant that researchers did not know much about CD4 counts, nor did they know that most of the conditions being used to diagnose them with AIDS, such as severe and chronic infections, are strongly associated with low CD4 counts, as are many other conditions that they were experiencing.

"Sporadic cases of apparent late-onset cellular immunodeficiency, associated with opportunistic infections, have appeared as case reports over the years. Because the emergence of HIV-associated AIDS coincided with the introduction of T-cell specific monoclonal antibodies which permitted the identification and quantitation of human CD4-positive T lymphocytes, no T-lymphocyte surface marker results are available on many of the earlier cases." (Bird 1996, page 172)

"Individual T-cell populations could not be quantified before 1978." (Bird 1996, page 173)

The first AIDS cases were identified in 1979, together with the extremely low CD4 counts that were thought to be the cause of their chronic infections. Because the tests used to measure CD4 counts were only developed the year before, in 1978, it is very likely that the assumption that HIV was causing the death of CD4 cells was made prematurely, before any clinicians or researchers had enough experience or knowledge about CD4 counts to make accurate decisions about their significance. Studies since that time on low CD4 counts have been widely ignored unless they focused on people diagnosed HIV-positive, creating the illusion that low CD4 counts are somehow specific to HIV and AIDS. This illusion may have allowed HIV to be falsely credited with creating immunodeficiency while other factors that are more significant are being ignored.


This review is extremely limited in scope, and many of the studies presented here use different measures of immune function, making it difficult to perform accurate comparisons. Nevertheless, it is remarkable that so many different conditions are associated with profoundly reduced CD4 counts, as well as reduced CD4 percentages, reduced measures of lymphocyte function, and reduced CD4/CD8 ratios. The fact that HIV-negative people with many common conditions like mononucleosis, pregnancy, and pneumonia can have levels below those needed to diagnose AIDS suggests that the common use of CD4 counts to make diagnostic and treatment decisions should be carefully reappraised, especially since most clinicians are apparently unaware of how serious these influences are. It is also apparent that the syndrome of AIDS, with extremely low CD4 counts and severe or fatal infections, is also fairly common in people diagnosed HIV-negative, and is likely to be present in between 40 and 70 percent of people admitted to intensive care units with severe acute or chronic infections (Feeney et al 1995, Williams et al. 1983). In people who die of their infections this percentage may be even higher.

Low CD4 counts and other immunosuppressive effects are associated with so many different physical and psychological stressors that it is possible that these other factors are the primary ones causing immunosuppression in many people diagnosed HIV-positive. Following is a brief list of factors commonly present in "high-risk" groups that could explain or contribute to a low CD4 count:

"1) In Africa, malnutrition, a variety of endemic infectious diseases, psychological stress, and social ostracism could all be strong factors in causing an acquired immunodeficiency.

2) In the United States and Europe, AIDS is still primarily confined to the original risk groups, male homosexuals, IV drug users, and hemophiliacs, all of whom regularly experience many of the conditions described:

a) Male homosexuals suffer from societal rejection which causes psychological stress and social isolation. When AIDS first appeared, several events had made the social isolation of male homosexuals painfully clear; a successful campaign to repeal gay rights in Miami Dade County was being led by Anita Bryant, and the first elected official in the United States who was openly gay, Harvey Milk, was assassinated. Ironically, over the years the phenomenon of AIDS may have helped significantly to reduce this social ostracism and hatred, albeit in the context of a widespread human tragedy.

b) The small subset of gay men in whom AIDS first appeared were engaging in a type of party atmosphere which involved multiple partners, late nights, and the regular use of alcohol and recreational drugs, possibly as a way to cope with the societal rejection they were experiencing. Many people in this group suffered from recurrent or chronic sexually transmitted diseases, as well as general ill health.

c) IV drug users live in conditions of psychological stress and social isolation, and also often suffer from malnutrition. Injections of foreign proteins are a daily routine, and opiates have also been shown to cause immunosuppression. IV drug users have always had high rates of infectious diseases including cellulitis, tuberculosis, pneumonia, and non-healing ulcers.

d) Hemophiliacs need regular transfusions of factor VIII, which introduces a number of foreign proteins and impurities into their bloodstream. The quality of the Factor VIII has steadily improved over the years, as has their health and life expectancy, but in spite of this they still have chronic health problems and their life expectancy is still greatly reduced when compared to the normal population.

e) Corticosteroids, which are cortisol analogues, are often used as treatments in people diagnosed HIV-positive, especially in Western nations, for illnesses such as pneumocystis carinii pneumonia (PCP).

3) The very diagnosis, HIV-positive, carries a substantial burden of psychological stress and social isolation, which is made even worse when the CD4 count is found to be reduced, or when "full blown" AIDS is diagnosed."

It would be helpful to see studies of CD4 counts in even more common illnesses like influenza, and to see studies that try to determine when the CD4 counts begin to fall. If the CD4 counts were low before experiencing the conditions presented, the CD4 count could have caused the condition. The low counts in burn and trauma victims, however, argue in favor of the hypothesis that the conditions themselves caused the low CD4 counts, as it is difficult to argue that such a high percentage of people had low CD4 counts before the trauma was experienced. The studies reviewed here show that the CD4 counts can stay low for weeks or months, and this effect would be magnified if many factors were present at once, or if several conditions occurred in sequential order. Because of this, repeated findings of low CD4 counts over time could also be a common finding.

Studies looking at the mechanisms that cause low CD4 counts could also be helpful. The hypotheses presented in some of the articles reviewed above regarding mechanisms include increased cortisol, antibody-mediated immune dominance, and malnutrition. It is possible that several of these could operate simultaneously, as well, or that they could occur sequentially in a cascade. All of the factors presented here, from infections to psychological stress, could combine in causing immunosuppression, and many of them could be much more easily treated than current methods of treating HIV, which rely on long-term use of medications with a number of serious adverse effects.

Finally, the results described here cast doubt on the original claims that HIV specifically targets CD4+ T lymphocytes. It could be instead that many or all of the conditions reviewed here operate under the same mechanism. The search for a new infectious agent began around 1979, when clinicians found extremely low CD4 counts in a few young male homosexuals who were dying of multiple infections. The ensuing international scientific search resulted in Robert Gallo's claim that HIV was the cause, in particular because it infected CD4+ lymphocytes (Gallo et al. 1984). Based on the results reviewed in above, however, it is very possible that the low CD4 counts in those early cases were simply a result of the opportunistic infections that were present, not because of any new agent that targeted CD4+ T-cells. This argument is strengthened by the continued difficulty in determining a mechanism for how HIV destroys CD4+ T-cells. The mechanisms originally proposed by Gallo have had to be abandoned, and new hypotheses have also experienced several major revisions over the years. A conference in 1997 determined that the cause was still unknown (Balter 1997), and recent articles seriously discredit the reigning hypothesis that the immune system destroys its own CD4+ T lymphocytes (Roederer 1998). A quote from the article by Balter (1997) which describes the conference on the causes of low CD4 counts, follows:

"It might be said that AIDS researchers know the virus that causes the disease, HIV, inside and out. They have isolated its proteins, sequenced its genome, and identified the receptors it uses to dock onto the CD4 T lymphocytes that are the viruses primary target. Yet the central mystery of AIDS remains unresolved: How does the virus cause the severe loss of CD4 T-cells, which wrecks the immune system, that is the hallmark of the disease?" (Balter 1997, page 1399)

One argument that is commonly used to support the claim that HIV specificically targets CD4+ cells is that when anti-HIV medications are given, the CD4 count rises. As described above in the section describing the immunosuppressive effects of anti-HIV medications, however, protease inibitors and AZT specifically inhibit a variety of microbes that commonly create infections in people diagnosed HIV-positive (PDR 1999, Cassone 1999, Atzori 2000). This finding may explain some of the rise in CD4 counts that people on these drugs experience, but there are also other important factors to consider such as the tremendous psychological relief that these drugs provide for those who take them. The introduction of protease inhibitors was accompanied by widespread media acclaim, and this may help them generate a powerful psychological effect that relieves much of the stress that is associated with the diagnosis HIV-positive. Because psychological stress lowers the CD4 count, its relief could allow the CD4 count to rise. Once a rise in the CD4 count is seen, for whatever reason, the relief of psychological stress would be strengthened, as would the belief in the power of the anti-HIV drugs.

About 5-15% of people who are diagnosed HIV-positive do not go on to show any immunological abnormalities at all, even after ten or more years (Learmont et al. 1992, Ashton et al. 1998, Walton 1999). In addition, only about 50% of people diagnosed HIV-positive will be diagnosed with AIDS in the first ten years after their diagnosis, a period which has been called the latent phase of the virus. Perhaps, by focusing on AIDS as a multifactorial illness, this latent phase can be extended indefinitely in more and more people. Furthur research that focuses on some of the many factors reviewed in this paper may reveal why these long-term nonprogressors appear to stay healthy in spite of being diagnosed HIV-positive, and may help increase the percentage of people who succeed in doing so.

Matt Irwin MD is a family practice resident who wrote several literature reviews on HIV and AIDS while attending medical school at George Washington University. He also holds a Master's degree in social work from the Catholic University of America. In addition to his interest in alternative views of HIV and AIDS, he specializes in health promotion with nutritional, psychological, social, and spiritual interventions, as well as classical homeopathy. He has a practice near Washington, D.C.

[email protected]
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" We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake"
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Starkman MN, Gebarski SS, Berent S et al. (1992). Hippocampal formation volume, memory dysfunction, and cortisol levels in patients with Cushing's syndrome. Biological Psychiatry; 32: 756-765.

Stefanski V, Engler H (1998 Jul). Effects of acute and chronic social stress on blood cellular immunity in rats. Physiol Behav;64(5):733-41

United States Pharmacopeial Convention (1996). USP DI: Drug Information for the Health Care Professional, 16th Edition. pages 3032-3034.

Verde TJ, Thomas SG, Moore RW, et al. (1992). Immune responses and increased training of the elite athlete. J Appl Physiol; 73(4); 1494-9.

Verges B, Chavanet P, Desgres J, Vaillant G, Waldner A, Brun JM, Putelat R (1989 Nov). Adrenal function in HIV infected patients. Acta Endocrinol (Copenh);121(5):633-7.

Walton C (1999). What makes a survivor? Continuum 5(5); 16-18.

Williams RC, Koster FT, Kilpatrick KA (1983, November). Alterations in lymphocyte cell surface markers in various human infections. Am J Med: Volume 75; 807-816.

Sorry R, I know that is a ton of reading...but i think it is safe to say that so called HIV is not found in a high enough % of AIDS cases to satisfy Kochs Postulates.

In addition to this there is the issue of the % of CD-4's that are infected by so called HIV. In an asymptomatic patient there is only about 1 in 10,000 CD-4 immune cells infected by this so called HIV. Even in an AIDS patient that has just died only about 1 CD-4 cell in 40 is infected by this so called HIV. That only represents about 2-3 percent of total CD-4's which is far to few to cause any damage. It takes at least 30% infection of the targeted cells to cause disease in other viral infections (ask any infectious disease specialist or doctor). Not to mention there is not proof of any *retrovirus* ever being cytocidal. They are viruses that by definition grow tumors.

Something else that is important to note is that about 99% of so called HIV that exists in the body is *non-infectious* virus-it lacks the gp120 *spikes* or *knobs* that is required to latch onto and infect the cd-4 lymphocyte. This is according to Robert gallo himself-he is the one that put forth this bizarre notion that HIV is the sole cause of AIDS.

I have more to post, but alas it is getting late. I will respond to your post about the NAT methods that your company uses tomarrow or the day after. Before I sign off, I will wrap up my belief in regards to HIV and AIDS-and this belief is put forth bu almost 2000 doctors and scientists around the world. This is The Group For The Scientific Reappraisal Of AIDS.

In the early 1980's there were large groups of gay men that got sick. It was because of their lifestyle-hard drugs and hard sex. We heterosexuals don't understand the gay underworld because we are not part of it. During the Disco era these gay males consumed every rec drug on the planet and had sex orgies on a regular basis. You should read some of the literature put forth by writers that were either part of that underworld or observed it. Sex parties where rec drugs kept these people up (in more ways than one) for days and anal sex with tens of partners in these few days. The nitate poppers relax the sphincter to facilitate anal sex-using this drug on a frequent basis will prevent males from achieving erections without it. Poppers have been directly linked to Kaposi's Sarcoma-which was the first AIDS defining disease. Gallo has since said that HIV has nothing to do with Kaposi's-it is all about poppers. And this was the number one AIDS defining disease of that era.

When immunity is compromised by whatever means it makes one susceptible to testing positive on an HIV antibody test. It is well known that people in Africa and India have higher immune circulating complexes that do caucasians and Europeans. This increases the chances of them testing positive.

And when someone tests positive they are put on the most toxic drugs on the planet. It is chemotherapy that is too toxic for cancer petients who would only use it for 2-3 weeks. AIDS people are told to take it the rest of their lives-no wonder they die.

I am sure you will disagree with me-no problem. I enjoy the discussion. But I seriously doubt there can be a vaccine for something that is yet to be proven to exist by means of classical virology. Bob Gallo said in 1984 that there would be a vaccine in 2 years. That was 18 years and 130 billion dollars ago....and the AIDS machine rolls on.
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Old 01-07-2005, 01:55 AM   #40
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Whew, I'm going to have to take time and read those articles. I do appreciate the articles as I read them.

Again, I think we could go on forever debating this and going back and forth posting relevant articles. The bottom line is that AGAIN we'll have to agree to disagree. For me, like I stated in my last post the many instances where biotech technicians have cloned the HIV virus and then autoinoculated themselves unintentially....and then tested postive for HIV and then DIED of AIDS is enough for me. With no other risk factors...third world disease, IV drug use, anal sex, or multiple partners. They cloned a virus.....and then got the disease...They all died of the virus that I can test and isolate using NAT. I applaud you in your fight, and incourage you to use the methods you believe in. I will do the same using the technology and science I belive in. Maybe someday we collectivley as a people can come to a cure for this dreaded disease whatever the name you choose to call this. However I think we should move this thread to the prevention forum as it has a ton of information for people to read. And maybe we could continue our discussion there or I think its only you and me that are interested and reading those articles.....or at least the only nerds that are responding I'm off to bed, and will print your articles to read tomorrow....thanks. Please pass on the article I posted from my collegues to your friends....I'm curious to see their view....or at least what they come up to try to disprove the technique. :p Also, where the hell do you live...I travel every few months for work....I'd love to sit down and talk shop with you one day.


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Old 01-07-2005, 06:24 AM   #41
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Need the condensed version of this. Appears interesting but the eyes and attention was straining after the 3 page down.
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Old 01-07-2005, 05:38 PM   #42
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WOW! talking about generating some DAMN GOOD INFO..jeeez -- SS, you da man!
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Old 01-07-2005, 09:01 PM   #43
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WOW I haven't read it all ..but will in the next day or so...hey we really managed to take this thread off the beaten path!

Quote from Peter Duesberg paraphrased " According to our Gov't, if you are HIV postive and suffer have AIDS...if you suffer dementia and are HIV negative ....then you are just STUPID !" Some funny shit!
This girls walks up to me and says " My God you're good looking!"

I say" I know!"

She gets offended and says" WHAT?!"

I said " I know I am goodlooking!"

She said " You're also and ASSHOLE!"

I said " I know that too!"
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Old 01-11-2005, 08:16 PM   #44
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I just wanted to reply to your last post, put up a little something about *HIV* and then readdress some more of the things Sweat mentioned in the original post.

BTW-I live in Carolina Beach,NC. I am on a small barrier island in SouthEast NC, about 45 minutes north of Myrtle Beach. If you ever head to the *traiangle* area-as in Triangle Research Park (Raliegh-Durham,NC) just let me know. The MD that I see there is the one that does the Ultraviolet Blood Irradiation treatments in conjuction with intravenous H2O2 administration, EDTA Chelation, etc. Give me a couple weeks heads up and I can meet you at his office and you can check out the UBI treatment *in vivo* with me as the patient (I use that term loosely as I suffer from nothing but occasional sleep deprivation). I use all of these therapies as part of my health and wellness program. mentioned you know of some people who inadvertly *infected* themselves with HIV and progressed to AIDS and died. Unfortunately this does happen, but is completely convoluted in regards to what actually happens. Here is what happens-

"One suprisingly and mildly reassuring fact is that when health workers were examined after needstick wounds only one out of 1500 in the UK and the US became infected " (reported by Drs Jorge Eichberg and Krishna Murthy, of The Southwest Foundation for Biomedical Research).

Now-we also know that there are at least 66 reasons that cause a positive reaction on an antibody test without anyprescence of so called HIV or HIV antibodies. Here is a thread that identifies each and every one, fully referenced-

It is very possible that this one in 1500 that tests positive is having a cross reaction from something other than this so called HIV or its antibodies.

Also consider that without having an isolated HIV that it is impossible to have a gold standard to test against. So even though the test kit manufactures say their test is 99% specific, well, that is impossible to tell-because there is no gold standard.

Also-these tests are not standardized. This means that a blood sample could be taken to 2 or more different labs and get 3 different results-positive, negative, or *indeterminate*. Also, depending on which country you get tested in makes a world of difference. In the US it takes 2-3 antigens to react for a positive test, Australia it takes 4, Africa it takes only one. The whole African thing is a rip because these people suffer from hypergammaglobulinemia-which is elevated antibodies in general. Plus it only takes one antigen to make the test react *positive* and there is no subsequent test to verify the first. The Africans only use the ELISA, which is too sensitive anyway, and the less sensitive Western Blot is not used to confirm the ELISA like in Europe and America. Consider that in Russia in 1992 there were 30,000 poitive on the ELISA but only 66 were confirmed positive by Western Blot. I am tellin ya, these tests are junk. And-get this-very rarely are tests even conducted in Africa. If an African shows up in a hospital AND HAS LOST 10% OF HIS/HER WEIGHT THEY ARE WRITTEN UP AS HAVING AIDS. Wow. Talk about pouring on the pseudoscience. Same thing happens if they have a fever or diarrhea. Of course no one wants to take in consideration that the Africans have parasites, TB, Dengue fever, for centuries. Everyone just wants to sell drugs. Keep that cash register running full speed...
As I always say-if you are thinking of getting an HIV antibody test done for whatever reason, well, go to Australia-you have a better chance of being negative.

Check this out-one of the scientists I correspond with -Christopher Tyler (he partakes in the BMJ debate and is a moderator at AIDSMYTHEXPOSED.COM) found this on *The* (another crap site sponsored by Big Pharma) and get a load of this in regards to the testing-

While doing some research I came across this little gem from our favorite website,, bastion of all things drug sponsored. A google search turned up this post from the questions section. Please note the thorough and complete and satisfying answer by one of their knowledgeable 'HIV' experts.

The heading was titled, 'Gold Standard' and posted back in 2001.

I just laughed when I came across this.



Hey Doc,

Why is there no Gold Standard when testing for the presence of HIV? Instead of looking for antibodies thought to be exclusive to HIV, wouldn't it be better to isolate actual virus in a suspected HIV+ person?

Why are the standards of testing and diagnosis different in most countries to that of the US? If I test positive in the US, I may not test postive in let's say Canada or the UK. Don't you think that's odd?

Are the tests standard in most countries for diseases like, let's say, Chicken Pox or Hepatitis?

Dr. Mark Holodniy, Stanford University, School of Medicine
I cannot answer why testing is not standardized.

Yeah, no kidding Mr. Holodniy. Nobody can answer that but anytime you turn on the TV you see or hear *Get tested! Find out now!,etc......

The follies of Bob Gallo will haunt this generation forever i do believe. lol. let's say a lab worker sticks themself and turns up *positive* for whatever reason. Let's look at what happens as per recommendation by the CDC, FDA, et al...

Let's say our lab worker's name is Jim. Jim is now positive, and the poor guy is certainly freaking out. Of course this has an effect on the body (mind-body relationship). As I posted above in Dr. Irwin's paper about Idiopathic T-cell Lymphocytopenia (AIDS w/ no HIV) sooner or later Jim will get his t-cell count tested and it will be low. Maybe he had some undue stress, or a flu virus, or whatever. His doc will then prescribe AZT and the HAART (Highly Active Anti-Retroviral Therapy) protease enzyme inhibitors. This will be to kill off the *virus* to spare his few remaining cd-4 cells, even though (as in Irwin's paper) it is well established that perfectly healthy people have low cd-4 counts.
As I mentioned in an earlier post, AZT is chemotherapy-it is a DNA chain terminator. Any cell that is actively replicating in the prescence of AZT will be killed, no questions asked. It just mows everything down. Now-let's say Jim only has 1 cd-4 that is infected out of 500. By using AZT-the most toxic drug on the planet-to kill the one *infected* cd-4 immune cell the other 499 UNinfected cells will also be killed. That means IF this HIV causes AIDS (by killing CD-4 immune cells) then AZT is some 499x more deadly than is *HIV*.

I like what Dr. Peter Deusberg has said about chemotherapy-

"Using chemotherapy is like going bunny hunting with an atomic bomb. Sure, you will get some bunnies, but the forrest doesn't look so good afterwards."

As mentioned by someone earlier, Deusberg has an uncommon wit and humor that isn't often found in nerdy science sleuths.

At any rate, our friend Jim is struggling with this drug regimen. His good meaning doctor has told him it is all there is for this *virus*. Meanwhile his digestive system is being crushed by AZT, his bone marrow is failing, the protease inhibitors are destroying his liver....and after about 18 months Jim dies. His offical cause of death-liver failure (this is what most AIDS patients die from) is attributed to AIDS. But the caveat is that HIV does nothing to the liver-it (according to the mainstream) only kills CD-4 immune cells, which are not liver cells.
IMO (and a hell of alot of other people) these AIDS deaths are iatrogenically induced by well meaning MD's with AZT and other HAART medications.
Anyone that thinks other wise well, I would direct you to AIDSMYTHEXPOSED.COM. This is a message board that is made up of scientists, MD's, journalists, investigators (such as I), concerned citizens, etc....and a hell of alot of people deemd *HIV positive*. None of them use the *antivirals* and none of the HIV positive people develop AIDS. There are many on that board that have given their life story and have beat this so called HIV for 2 decades. Alot of them had been on the Rx antivirals and after being almost dead, told their MD to take a hike, and have regained their health. Some swear that they never fully recover from AZT posioning.

R-I know you believe in your NAT testing. So we disagree-not a big deal. Makes for stimulating convo's b/n people like us that hopefully will educate others along the way.
But I doubt NAT testing will replace antibody testing b/c there will surely be some discordance. And that discordance will cause alot of grief for the ProHIV establishment. They already can't explain why it is that 3-7% of the HIV neg population shows prescence of so called HIV by PCR.
The follies of Bob Gallo......

At any rate, we probably won't use NAT or PCR in our experiment this summer-but thanks for offering some test kits. The only test kit we will use is the Western Blot antibody test. As it syands now, and has for over 15 years, a person gets tested by the ELISA first. If that is pos then the patient comes back for the Western. If the Western is pos, then they are told they are infected with the crud of the century. If the western comes back neg, then they are *HIV free*. Hence, our only concern is the Western.

Anyway, I will close this post by citing a paper written by Dr. Kary Mullis. Mullis is a Nobel Prize winner for his invention of Polymerase Chain reation (PCR). He says his device is incapable of being of use in HIV technology because there is no isolated HIV. For people that do not know what PCR is, well this is what scientists use to amplify genetic material. It is *biotech's zerox copier*. Ever seen a cop show where they find a speckle of blood or semen and use it for DNA testing? They use Mullis' invention of PCR to amplify the genetic material so there is enough to run standard lab proceedures to catch a murderer, rapist, or identify a victim.
As you read this paper take in consideration that Dr. Mullis is a Nobel winner-the undisputed Holy Grail in science. He could not find a reference when writing a paper 15 years ago where someone proved HIV caused AIDS. At all the conferences he went o he asked anyone that gave a speech about HIV as to where exactly was the paper that proved HIV caused AIDS. No one could answer him. He even approached Dr. Luc Montegnier who actually discovered this so called HIV. Mullis asked Montegnier point blank in front of other scientists as to where was the proof that HIV causes AIDS. You will see what kind of answer he got. And if a Nobel Prize winner can't get an answer, well none of us probably will either.

This article is the Foreword that Mullis wrote for Dr. Peter Deusberg's book titled " Inventing the AIDS Virus"


By Kary Mullis

In 1988 I was working as a consultant at Specialty Labs in Santa Monica, setting up analytic routines for the Human Immunodeficiency Virus (HIV). I knew a lot about setting up analytic routines for anything with nucleic acids in it because I had invented the Polymerase Chain Reaction. That's why they had hired me.

Acquired Immune Deficiency Syndrome (AIDS), on the other hand, was something I did not know a lot about. Thus, when I found myself writing a report on our progress and goals for the project, sponsored by the National Institutes of Health, I recog nized that I did not know the scientific reference to support a statement I had just written: "HIV is the probable cause of AIDS."

So I turned to the virologist at the next desk, a reliable and competent fellow, and asked him for the reference. He said I didn't need one. I disagreed. While it's true that certain scientific discov eries or techniques are so well established that their sources are no longer referenced in the contemporary literature, that didn't seem to be the case with the HIV/AIDS connection. It was totally remarkable to me that the individual who had discovered the cause of a deadly and as-yet-uncured disease would not be con tinually referenced in the scientific papers until that disease was cured and forgotten. But as I would soon learn, the name of that individual - who would surely be Nobel material - was on the tip of no one's tongue.

Of course, this simple reference had to be out there somewhere. Otherwise tens of thousands of public servants and esteemed scientists of many callings, trying to solve the tragic deaths of a large number of homosexual and/or intravenous (IV) drug-using men between the ages of twenty-five and forty, would not have allowed their research to settle into one narrow channel of investigation. Everyone wouldn't fish in the same pond unless it was well estab lished that all the other ponds were empty. There had to be a pub lished paper, or perhaps several of them, which taken together indicated that HIV was the probable cause of AIDS. There just had to be.

I did computer searches, but came up with nothing. Of course, you can miss something important in computer searches by not putting in just the right key words. To be certain about a scientific issue, it's best to ask other scientists directly. That's one thing that scientific conferences in faraway places with nice beaches are for.

I was going to a lot of meetings and conferences as part of my job. I got in the habit of approaching anyone who gave a talk about AIDS and asking him or her what reference I should quote for that increasingly problematic statement, "HIV is the probable cause of AIDS."

After ten or fifteen meetings over a couple years, I was getting pretty upset when no one could cite the reference. I didn't like the ugly conclusion that was forming in my mind: The entire campaign against a disease increasingly regarded as a twentieth century Black Plague was based on a hypothesis whose origins no one could recall. That defied both scientific and common sense.

Finally, I had an opportunity to question one of the giants in HIV and AIDS research, Dr Luc Montagnier of the Pasteur Institute, when he gave a talk in San Diego. It would be the last time I would be able to ask my little question without showing anger, and I figured Montagnier would know the answer. So I asked him.

With a look of condescending puzzlement, Montagnier said, "Why don't you quote the report from the Centers for Disease Control? "

I replied, "It doesn't really address the issue of whether or not HIV is the probable cause of AIDS, does it?"

"No," he admitted, no doubt wondering when I would just go away. He looked for support to the little circle of people around him, but they were all awaiting a more definitive response, like I was.

"Why don't you quote the work on SIV [Simian Immunodeficiency Virus]?" the good doctor offered.

"I read that too, Dr Montagnier," I responded. "What happened to those monkeys didn't remind me of AIDS. Besides, that paper was just published only a couple of months ago. I'm looking for the original paper where somebody showed that HIV caused AIDS.

This time, Dr Montagnier's response was to walk quickly away to greet an acquaintance across the room.

Cut to the scene inside my car just a few years ago. I was driving from Mendocino to San Diego. Like everyone else by now, I knew a lot more about AIDS than I wanted to. But I still didn't know who had determined that it was caused by HIV. Getting sleepy as I came over the San Bernardino Mountains, I switched on the radio and tuned in a guy who was talking about AIDS. His name was Peter Duesberg, and he was a prominent virologist at Berkeley. I'd heard of him, but had never read his papers or heard him speak. But I listened, now wide awake, while he explained exactly why I was having so much trouble finding the references that linked HIV to AIDS. There weren't any. No one had ever proved that HIV causes AIDS. When I got home, I invited Duesberg down to San Diego to present his ideas to a meeting of the American Association for Chemistry. Mostly skeptical at first, the audience stayed for the lecture, and then an hour of questions, and then stayed talking to each other until requested to clear the room. Everyone left with more questions than they had brought.

I like and respect Peter Duesberg. I don't think he knows necessarily what causes AIDS; we have disagreements about that. But we're both certain about what doesn't cause AIDS.

We have not been able to discover any good reasons why most of the people on earth believe that AIDS is a disease caused by a virus called HIV. There is simply no scientific evidence demonstrating that this is true.

We have also not been able to discover why doctors prescribe a toxic drug called AZT (Zidovudine) to people who have no other complaint than the presence of antibodies to HIV in their blood. In fact, we cannot understand why humans would take that drug for any reason.

We cannot understand how all this madness came about, and having both lived in Berkeley, we've seen some strange things indeed. We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake.

I say this rather strongly as a warning. Duesberg has been saying it for a long time.*
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" We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake"
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Old 01-11-2005, 08:34 PM   #45
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As for our food dupply being poisoned, well read these threads and judge for yourself-
Aspartame and sudden heart attacks-

Genetically Modified Foods (scary stuff)
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" We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake"
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"The fact is that you can not start off with bad science and end up with good medicine"

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Old 01-11-2005, 09:13 PM   #46
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I'll be sure to travel sometime out there. If I do we should have a sit down.

As for your post. The transmission and death I spoke of earlier is of documented researchers that cloned the virus and then transmitted it to them selves inadvertantly. Can I ask to every explanation why are you so quick to post articles that are a tangent of what we were discussing....i.e. the british study....doesn't disprove just takes up space? Again about the transmission, they had a virus they isolated and in early studies it was cultured...then they got exposed. Tested positive...I beileve 6, did...they all died.

That is all the proof I need. If anyone would like me to clone a virus that I have so called named "HIV" and then expose your mucosal lining to it and see if you don't get aids...let me know. Bottom line, regardless of the tons of pages of HIV infection without any other "lifestyle" causes...or any sex, or any iv to a human, will cause AIDS and kill you. If you want to call it another name....sure go ahead. I'll continue working on this virus...I've had enough of the article swapping....obviously you don't read them...nor does anyone I'm not going to post them.

And forgive me for being brief and blunt, but I just started my prep and my brain cells are jello after a day of work. My Opinon, and I'm getting to feel i'm alone on that our memebers here, well from at least this threads and threads in the past, will think that HIV is not real. That a shower will kill you, and that the govt., pharma, and every other entitiy is out to get you. In reality its just not that black and white. Kevin Tredue is not going to save anyone...hes a quack artist....he's out for money...and true so are the pharma compaines....this is America though right? I really think people should think through things.....before you just start tossing out modern medicne...and the truth that if infected by a person with most likley will die. You might not test positive for a while, you might and then it might take a therapy i.e. H202 that because of its chemical interaction give you a false positive test. Bottom line is you will die....if your the 1 out of 1 million that survive or have some miracle clearance of does happen now....consider your a genetic anomoly and won the lotto....the rest of us will be dead. These cures if real, wouldn't be found solely on Intensemuscle, or by a few doctors around the world. This is America...if it worked, it would be on the shelves....too much money to pass up. I'll put on my flame suit now and go back to my prep....but I'm done with this discussion.


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Old 01-11-2005, 10:47 PM   #47
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Hhhmmm. Seems as though I struck a nerve. Sorry bout that. I thought it was a good, informative discussion. Gets lots of views, that is for sure.

Do you not see some gaping holes in this HIV as sole cause of AIDS hypothesis?

You can get me to shut up real quick like by doing these things-

1-Post an Electron Micrograph of isolated *HIV*. Please do not entertain me with the computer generated images of what HIV is supposed to look like. I want to see the real deal. This EM must also have the researchers name attached to it and the lab where it was isolated. It must be from an UNcultured sample and must exhibit the morphology of a retrovirus. That will get us off to a start in proving that HIV exists...

2- Post the original document where someone proved that HIV caused AIDS .

3-Explain how a *virus* that that at most infects a mere 2-3% of total cd-4 cells causes total immune collapse.

4-explain why it is in Gallo's papers submitted to Science in May 1984 that only 36% of AIDS patients showed prescence of so called HIV. What caused AIDS in the other 64% of AIDS patients that had no prescence of *HIV*.
Is it not unreasonable to think what caused AIDS in the 64% group also caused AIDS in the 36% group?

To top that off the *prescence of HIV* that gallo used was p41. No researcher regards p41 as anything of any significance because it is a componet in actin, which is found in everyone.

5- If HIV is the sole causative agent in AIDS why is it that there are thousands-even millions-of cases of AIDS with NO HIV detected?

6- Why is it that no one-not Robert Gallo or Luc Montegnier - has ever been awarded the Nobel Prize for any of this *HIV science*. After all Montegneir discovered it and Gallo developed the antibody testing that *has saved millions*. If any of the mainstream HIV science is so true why has nobody won the Nobel for it?

Could it be because scientists on the inside know that it is all a scam??

6-Explain to me why it is that people such as Christine Maggoirre (who owns the website and Kim Bannon (who is taking the test kit manufacturer to court) have been so called HIV positive since 1992 or earlier and have not developed any kind of sickness that could possibly be interpreted as AIDS.

7-Explain this new syndrome called Immune Restoration Dysfuntion (IRD). This is where an *HIV pos AIDS * patient is given drugs to restore the immune system. Viral load disappears and CD-4 counts go up to normal. But the patient dies anyway. How can that happen if so called HIV is practically eradicated?

Sorry R-but I want to see scientific evidence that proves beyond a shadow of a doubt that HIV exists and does in fact cause AIDS.

Just because the majority of HIV positive people go on to develop AIDS does not mean that HIV causes AIDS. Correlation is not proof of causation. After all, 100% of AIDS patients show prescence of antibodies to Candida Albicans-but can anyone say that Candida is the cause of AIDS?

As for the therapies I have written about-alot more than just a few doctors around the world use them. Hundreds use them in Germany, and thousands in Russia. Just because you have never heard of them does not make them false.

You do know that Chiropractic practitioners experienced the same kind of treatment by the *establishment* correct? Same with acupuncturists correct? Look at those fields of medicine-that is real medicine my friend.

It is attitudes like yours that relegate American Medicine to its ranking of number 37 in the world by the WHO. Despite the fact that we spend more money on health care than any other nation. And our life expectancy is number 24 according to WHO.

The American ignorance spurns the American arrogance in medicine. Or is it the other way around??
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" We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake"
Dr. Kary Mullis, Nobel Prize Winner in Chemistry for inventing the Polymerase Chain Reaction

"The fact is that you can not start off with bad science and end up with good medicine"

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Old 01-12-2005, 12:07 PM   #48
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<<Could it be because scientists on the inside know that it is all a scam??>>

You right, the 50,000 employees combined of Chiron, Genentech, and Amgen (whom all work on the HIV vaccine) are holding back a conspiracy. Your right, we've all collectively decided to hide the truth, throw our graduate and PhD degrees out the window and lie to the public. Thanks for solely being the voice of truth.........

<<Hhhmmm. Seems as though I struck a nerve. Sorry bout that. I thought it was a good, informative discussion. Gets lots of views, that is for sure.>>

No you have not struck a nerve, it is a potentially harmful view to put out there...and that is dangerous. And I believe its doing our members a disservice......we have a ton of new members those whom are practically young and not in the medical field. For you to put out the idea so vehemently that HIV does not cause AIDS is unethical and potentially harmful to someone who takes that message home and feels "well, its a lifestyle disease...if I don't mainline or sleep with homosexuals I'll be okay"'ll be dead if the other person has HIV.

<<Sorry R-but I want to see scientific evidence that proves beyond a shadow of a doubt that HIV exists and does in fact cause AIDS.>>

Of course there is not SOLID evidence that HIV causes AIDS....but there is a strong enough correlation. Hell we don't understand Cancer, Parkinson's, or the basic function of the cell at the molecular level. You know that just because something is not found on a test it does not mean it is not there. And for the sake of argument...lets say its not HIV. The fact is that there is a virus, that can be found to test positive using nucleic acid testing....I can take the genetic structure of that virus and culture it. And guess what, if injected or if it comes into contact with a mucosal lining.....I develop the symptoms and eventually die from it from a immune disorder. This virus dna protein can be found in most ALL cases of those whom test positive for HIV. If you want to name it something else...fine...but in the real world it is there and it will kill you. We can debate theories all day...there is an article and study for everything...what we need to look at is what is reputable and more important what is RELEVANT to the discussion.

<<Just because the majority of HIV positive people go on to develop AIDS does not mean that HIV causes AIDS. Correlation is not proof of causation. After all, 100% of AIDS patients show presence of antibodies to Candida Albicans-but can anyone say that Candida is the cause of AIDS?>>

Agreed to a point. Correlation is not proof of causation. But, when boosted with a controlled drug delivery i.e. microparticles, or sustained release of an "HIV vaccine" which takes the gag-pol and gag envelope of the viruses DNA we have seen an antibody response to this that has kept macaques and chimps from developing a primate version of AIDS. Sure it is not absolute proof, but it does show that neutralization of this said virus halts the onset of AIDS. I believe in the last discussion on HIV I posted these studies.

Then there are the hundreds of real world cases where a virus found in the blood supply was transmitted to children, men, and women through blood transfusion. Children whom exhibited no risk factors i.e. drug use, sex, became infected and died of what we call AIDS.

<<It is attitudes like yours that relegate American Medicine to its ranking of number 37 in the world by the WHO. Despite the fact that we spend more money on health care than any other nation. And our life expectancy is number 24 according to WHO.>>

No it is attitudes like mine that give a reality check to some of the conspiracy theories and quackery that's out there. My attitude has nothing to do with our life expectancy....really, where do you come up with this stuff....Come on now, you have got to know that the difference in life expectancy is based on our food system...not our health care. You look at the avg. Americans diet and those of the top ranking countries with high life expectancies and you'll see it clear as day. Its McD's and our super sizing of everything that kill us early........not my attitude.


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Old 01-12-2005, 11:23 PM   #49
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Quite an interesting read SS....where do you get your information, if you don't mind me asking?
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Old 01-13-2005, 09:02 AM   #50
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Originally Posted by wannabbig
Quite an interesting read SS....where do you get your information, if you don't mind me asking?

I have quite a few sources. I correspond with several scientists and MD's that make up an organization called "The Scientific Group For The Reappraisal of AIDS". This is a membership of almost 2000 scientists and doctors that believe HIV is not the cause of AIDS. Of the group I have a keen interest in what the researchers and MD's from the *Perth Group* of The Royal Perth Hospital in Western Austrailia. I also correspond with the group's president -Dr. Roberto Giraldo,MD.

The Group's website is There are about 800 or more scientific papers published at this site that diaprove the HIV/AIDS myth.
Another source is a large group of people that make up the message board *AIDSMYTHEXPOSED.COM This is a diverse board made up of scientists, doctors, journalists, investigators (such as I) and alot of people deemed *HIV positive* from all over the world. A phenomenal resorce. I correspond a fair bit with one of the moderators, Christopher Tyler, who also partakes in the Great Debate on the British Medical Journal's website. This is a debate among scientists,doctors, and concerned citizens on both sides-The *ProHIV group* and *The AIDS ReThinkers*.

I also correspond with Dr. Wilhelm Godshalk,PHD, of the Netherlands in regards to this HIV thing.

I too believed the ideas that xRAJAx has written about until about January of 2000. Then I met an AIDS patient at an MD's office that I infrequently visit-after a 4 hour conversation with her (she has been HIV pos since about 1986) I looked into this whole HIV thing for a good 6 months-and after looking at the science (or lack thereof) from both sides I made up my own mind that there is no possible way that HIV causes AIDS, and I am very dubious that HIV even exists.

From my investigation of diseases like Candidaisis-which more often than not is determined by antibody testing-I knew that using an antibody test for prescence of *virus* is flawed. Not only that, but I began working on a *protocol* that would seroconvert a person from HIV positive to negative. These antibody tests only react positively when antibody levels meet the threshold. There is a very good chance that we all have these antibodies. Here is a paper authored by the President of The Group For The Reappraisal of AIDS-

I will be back later tonite to address xRAJAx's last post-

I respectfully submit "Everyone Tests Positive For HIV"

Everyone Reacts Positive
on the ELISA Tests for HIV

This is an article first published in Continuum (London) Winter 1998/9 5(5): 8-10

For the last 6 years I have been working at a laboratory of clinical immunology in one of the most prestigious University Hospitals in the City of New York. Here I have had the opportunity to personally run and get to know in detail the current tests used for the diagnosis of HIV status, namely, the ELISA, Western blot and Viral Load tests.

1. Diluting the serum for the ELISA test

The ELISA test is a test for antibodies against what is supposed to be the Human Immunodeficiency Virus or HIV. To run this test, an individual’s serum has to be diluted to a ratio of 1:400 with a special specimen diluent. According to the test kit manufacturer this diluent contains "0.1% triton X-100, Bovine and Goat Sera (minimum concentration of 5%) and Human T-Lymphocyte Lysate (minimum titer 1:7500). Preservative: 0.1% Sodium Azide" (1).

This extraordinarily high dilution of the person’s serum [400 times] took me by surprise. Most serologic tests that look for the presence of antibodies against germs uses neat serum [undiluted]. For example, the tests that look for antibodies to hepatitis A and B viruses, rubella virus, syphilis, hystoplasma and cryptococus, to mention a few of them, use straight serum [undiluted]. However, to try to prevent false positive reactions some serologic tests use diluted serum; for example this is the case with tests that look for antibodies to measles, varicella and mumps viruses which use a dilution of 1:16, to cytomegalovirus [CMV] 1:20 and to Epstein-Barr Virus [EBV] 1:10.

The obvious questions are: What makes HIV so unique that the test serum needs to be diluted 400 times? And what would happen if the individual’s serum is not diluted ?

2. Testing the ELISA test without diluting the serum

To answer these questions I ran an experiment in a medical laboratory in Yorktown Heights, New York. I ran it using the same test kit reagents that are usually used to run the ELISA test in most clinical laboratories worldwide (1).

I first took samples of blood that, at 1:400 dilution, tested negative for antibodies to HIV. I then ran the exact same serum samples through the test again, but this time without diluting them. Tested straight, they all came positive.

Since that time I have run about 100 specimens and have always gotten the same result. I even ran my own blood which at 1:400 reacts negative. At 1:1 [undiluted] it reacted positive. I should mention that with the exception of my own blood, the patient samples all came from doctors who requested HIV tests. It is therefore likely that most of the blood samples that I tested belonged to individuals at risk for AIDS.

According to Abbott Laboratories, the absorbance value [yellow color intensity] "develops in proportion to the amount of antibodies to HIV-1 which is bound to the bead" (1). What I noticed is that the absorbance values of the specimens that tested negative when diluted [1:400], but positive when undiluted [1:1], had lower values that the samples that, diluted, react positive on both the ELISA and Western blot tests. This would probably mean that the blood that is negative when diluted but positive when undiluted has a lower level of antibodies than the diluted blood that is doubly positive and, therefore, may probably test negative on the Western blot test. However, I have not had the opportunity to check this hypothesis.

It is important to note that the Western blot antibody test for "HIV" also needs serum to be diluted. Although it too has an unusually high dilution, here the individual serum is only diluted at a ratio of 1:50 (2). I have not yet had the opportunity to run this test with undiluted [1:1] specimens.

3. Discussion

The following are three possible explanations for why undiluted specimens of blood always react positive at the ELISA test:

3.1. Everybody has HIV antibodies.

It is accepted worldwide that the ELISA test for HIV detects antibodies against what is known as the Human Immunodeficiency Virus (3-6). And the pharmaceutical company that commercializes the ELISA kits states that "Abbott HIVAB HIV-1 EIA is an in vitro qualitative Enzyme Immunoassay for the Detection of Antibody to Human Immunodeficiency Virus Type 1 (HIV-1) in Human Serum and Plasma" (1).

Since all undiluted blood specimens react positive on the ELISA test, a test that supposedly tests for antibodies to HIV, the results presented here suggest that every single human being has HIV antibodies. And this suggests that everybody has been exposed to HIV antigens.

This would mean that all of us have been exposed to the virus that is believed to be the cause of AIDS. The people that react positive even at a dilution of 1:400, would be the ones that have had the highest level of exposure to HIV antigens. The rest of the people - the ones that only react positive with undiluted serum [1:1] - would have had a lower level of exposure to HIV.

3.2. Everybody has different levels of HIV infection.

It is also believed worldwide that a person that reacts positive for antibodies against HIV has not only been exposed to but is infected with a deadly virus that causes immunedeficiency (3-6). Therefore, the positive reactions of all undiluted serums would mean that everybody, or at least all the blood samples that I have tested, including my own, are infected with this "deadly" virus. The ones that react positive at a ratio of 1:400 would simply have a higher level of "deadly" infection than the "deadly" infection had by the ones that only react positive with undiluted serum.

3.3. The test is not specific for HIV.

The results presented here could also mean that the tests used for detecting antibodies to HIV are not specific for HIV, as has been explained previously (7-14). In this case, there would be reasons other than HIV infection, past or present, to explain why a person reacts positive to it. The test also reacts positive in the absence of HIV (7-14).

The scientific literature has documented more than 70 different reasons for getting a positive reaction other than past or present infection with HIV (7,10,11,14,15). All these conditions have in common a history of polyantigenic stimulations (15,16).

Even Abbott Laboratories is well aware of the specificity problems with the ELISA test. This is why they state: "EIA testing alone cannot be used to diagnose AIDS, even if the recommended investigation of reactive specimens suggests a high probability that the antibody to HIV-1 is present" and "Although for all clinical and public health applications of the EIA both the degree of risk for HIV-1 infection of the person studied and the degree of reactivity of the serum may be of value in interpreting the test, these correlations are imperfect. Therefore, in most settings it is appropriate to investigate repeatably reactive specimens by additional more specific or supplemental tests" (1). Interestingly, there are countries like Great Britain where the diagnosis of HIV status is based on the ELISA test alone. No Western blot or any other test is needed there.

The only proper way for establishing the sensitivity and specificity of a given test is with a gold standard. However, since HIV has never been isolated as an independent purified viral entity (17-19), there cannot be a gold standard for HIV. The sensitivity and specificity of the antibody tests for HIV have instead been defined based on the assumption that HIV is the cause of AIDS. In this way, "The Abbott studies show that: Sensitivity based on an assumed 100% prevalence of HIV-1 antibody in AIDS patients is estimated to be 100% (144 patients tested)" and "Specificity based on an assumed zero prevalence of HIV-1 in random donors is estimated to be 99.9% (4777 random donors tested)" (1). "At present there is no recognized standard for establishing the presence and absence of HIV-1 antibody in human blood. Therefore sensitivity was computed based on the clinical diagnosis of AIDS and specificity based on random donors" (1). [Emphasis is mine].

Since there is no scientific evidence that the ELISA test is specific for HIV antibodies, a reactive ELISA test at any concentration of the serum would mean presence of non-specific or polyspecific antibodies (20). These antibodies could be present in all blood samples. They are most likely a result of the stress response, having no relation to any retrovirus, let alone HIV (21,22). In this case, a reactive test could be a measure of the degree of one’s exposure to stressor or oxidizing agents (15,16).

The inevitable conclusion is that all positive reactions for antibodies to HIV are simply false positives. If nobody is positive for HIV, then people who react positive on the ELISA test do so due to something other than HIV.

4. Proposal to find out the real meaning of the "HIV antibody" tests

To uncover the meaning of these tests I propose a simple experiment: Take blood from three groups of people and run the tests highly diluted, undiluted and at a wide spectrum of dilutions in between. The first group would be a group of healthy people of many age groups; the second group would be a group of people from the conventional AIDS "risk groups"; the third group would be a group of people with clinical conditions both related and unrelated to AIDS. All groups would be subjected to both the ELISA and Western blot tests.

Additionally, all blood samples could be subjected to the "the viral load test for HIV".

The results of such an experiment could determine whether these test measurements bear any relationship to an individual’s level of exposure to stressor or oxidizing agents. If so, the tests could be salvaged as a measure of an individual’s level of intoxication.

Let us find the economic support necessary to run this experiment. In the mean time, since people are reacting positive on tests that are not specific for HIV, let’s please stop labeling them as "HIV positive".

5. Acknowledgments

I want to thank Mr. Albert Padovani, Director of Yorktown Medical Laboratory for permitting me to run the experiments reported here in his laboratory and for providing the reagents for the tests. Also I thank Tom DiFerdinando Executive Director of Health Education AIDS Liaison (HEAL) in New York City for editing the manuscript for this article and for his valuable suggestions.


ABBOTT LABORATORIES. Human Immunodeficiency Virus Type 1. HIVAB HIV-1 EIA. Abbott Laboratories, 66-8805/R5. January 1997: 5.

EPITOPE ORGANON TEKNIKA. Human Immunodeficiency Virus Type 1 (HIV-1). HIV-1 Western Blot Kit. PN201-3039 Revision # 6.

FEINBERG MA & VOLBERDING PA. Testing for Human Immunodeficiency Virus. In: COHEN PT, SANDE MA and VOLBERDING PA. The AIDS Knowledge Base. Boston: Little, Brown and Company, 1994: Section 2.

PINS MR, TERUYA J and STOWELL CP. Human Immunodeficiency Virus Testing and Case Definition: Pragmatic and Technical Issues. In: COTTON D and WATTS DH. The Medical Management of AIDS in Women. New York: John Wiley & Sons, 1997: 163-176.

METCALF JA, DAVEY RT and LANE HC. Acquired Immunodeficiency Syndrome: Serologic and Virologic Tests. In DEVITA VT, CURRAN J, HELLMAN S, et al. AIDS: Etiology, Diagnosis, Treatment and Prevention. 4th Edition. Philadelphia: Lippincott - Raven, 1997: 177-196.

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PAPADOPULOS-ELEOPULOS E, TURNER V & PAPADIMITRIOUS JM. Is a Positive Western Blot Proof of HIV Infection? Bio/Technology 1993; 11:696-707.

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HODGKINSON N. Science Fails the "AIDS Test" In: AIDS: The Failure of Contemporary Science. How a Virus that Never Was Deceived the World. London: Fourth Estate, 1996: 232-262.

JOHNSON C. Factors Known to Cause False-Positive HIV Antibody Test Results; Zenger’s San Diego, California, September 1996a: 8-9.

JOHNSON C. Whose Antibodies Are They Anyway? Continuum (London) September/October 1996b; 4(3):4-5.

TURNER VF. Do Antibody Tests Prove HIV Infection? Interview by Huw Christie Editor of Continuum. Continuum (London) Winter 1997/8; 5(2):10-19.

SHENTON J. Positively False: Wrong Tests and Long-Term Survivors. In: Positively False: Exposing the Myths around HIV and AIDS. London: I.B. Tauris, 1998: 238-239.

GIRALDO RA. Milking the Market. Will Mothers Dish Out the W.H.O. Formula? Continuum (London) 1998; 5(4):8-10.

PAPADOPULOS-ELEOPULOS E. Reappraisal of AIDS - Is the Oxidation Induced by the Risk Factors the Primary Cause? Medical Hypothesis 1988; 25:151-162.

GIRALDO RA. AIDS and Stressors II: A Proposal for the Pathogenesis of AIDS. In: AIDS and Stressors. Medellín, Colombia: Impresos Begón, 1997: 57-96.

PAPADOPULOS-ELEOPULOS E, TURNER V, PAPADIMITRIOU JM & CAUSER D. The Isolation of HIV: Has it Really Been Achieved? The Case Against. Continuum (London) 1996; 4(3):S1-S24.

LANKA S. No Viral Identification: No Cloning as Proof of Isolation. Continuum (London) 1997; 4(5):31-33.

DE HARVEN E. Remarks on Methods for Retroviral Isolation. Continuum (London) 1998; 5(3):20-21.

WING MG. The Molecular Basis for a Polyspecific Antibody. Clin Exp Immunol 1995; 99:313-315.

SNYDER HW and FLEISSNER E. Specificity of Human Antibodies to Oncovirus Glycoproteins: Recognition of Antigen by Natural Antibodies Directed Against Carbohydrate Structures. Proc Nat Acad Sci USA 1980; 77:1622-1626.

BARBACID M, BOLOGNESI d & AARONSON SA. Humans Have Antibodies Capable of Recognizing Oncoviral Glycoproteins: Demonstration that These Antibodies are Formed in Response to Cellular Modification of Glycoproteins Rather than as Consequence of Exposure to Virus. Proc Nat Acad Sci USA 1980; 77:1627-1621.
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" We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake"
Dr. Kary Mullis, Nobel Prize Winner in Chemistry for inventing the Polymerase Chain Reaction

"The fact is that you can not start off with bad science and end up with good medicine"

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