infectious vs oxidative stress theory of AIDS [very long!]
Tue, 30 Nov 1999 21:57:07 -0500

Sorry for the delay in replying to Hal's questions. Work, Thanksgiving, and I had to look up a lot of stuff.

>>Pat Fallon,
> >The HIV antibody test might simply be picking up on
> >human-produced “HIV” material. In this case, a positive
> >test would mean that cells of the body had been
> >sufficiently damaged to generate a reaction. A positive test
> >would be a marker of disease - not necessarily that
> >“HIV” is the cause of AIDS.

>Would this theory predict that AIDS is non-infectious?

The 30 or so diseases would each have their own classic cause. The diseases should be vigorously treated in their own right.

The only reason to group these established diseases together under the new syndrome AIDS was because it was thought an infectious retrovirus, HIV, was causing the immune system collapse
common to all these patients.

It is argued that it is not useful to group patients with one of 30 or so distinct, established diseases together into a new syndrome
until the proposed common causal virus has been isolated.

I would like to emphasize
what I think is an important point.
The seminal argument is this: If someone says HIV causes AIDS, they must begin by proving HIV exists.

There are well-established procedures to properly isolate a retrovirus,[1] which we ignore at considerable peril.

As I understand it, retrovirus are not esoteric, nuclear or cosmological notions whose postulated existence can only be inferred by indirect observations. They are particles which can be seen, though not with the naked eye. Since Montagnier and his colleagues admit to not seeing particles at the characteristic density having the morphology of retrovirus, to claim the presence of a retrovirus much less a "purified virus" is unsubstantiated.

In place of the logic and rigor
demanded by the steps referenced above, a series of nonspecific phenomena has been accepted as proof for the existence of HIV.

This is the first point The Perth Group made, in 1988.

IMHO, this fact is hard to avoid, and it has direct bearing on the questions you ask.

In addition to introducing an HIV critique based on the principal of viral isolation, Papadopulos also unveiled in her 1988 paper an explanation for AIDS based on the process of oxidative stress. According to Papadopulos, the stimulants used to induce "HIV" phenomena in cultures are oxidizing agents . As are the factors uniting American AIDS patients, including street drugs, hemophilia treatments, and rectally deposited semen. Papadopulos proposed that both "HIV" phenomena and AIDS conditions are consequences of these and other stressors she would introduce in later papers (such as blood transfusions, anti-AIDS pharmaceuticals including AZT, and antibiotics). In her view, when oxidation is prolonged or excessive, cells become abnormal, injured and susceptible to diseases.

>How would it explain the epidemiological trail seen in AIDS,
>which Steve Harris describe?  One infected person has sex
>with another, and then the other guy gets it?

Since "HIV" has not been isolated, the term "infected person" used in that context seems premature.

HIV/AIDS is claimed to be sexually transmitted. Data to support this claim is based not upon microbial isolation and contact tracing as is the orthodox practice for proving diseases are infectious and sexually transmitted, but on tests for antibodies in blood which react to certain proteins deemed but not proven to be "HIV specific".

Oxidative stress produces these effects with no infectious agent.

Too bad the proponents of the infectious HIV/AIDS model cannot produce the micrographs of proper viral isolates. In the absence of clear proof, we can look at the predictions each theory of AIDS makes. The two theories would make different predictions.

The theory that AIDS is caused by a sexually transmitted infectious retrovirus with a 10 year latency period would
[and did]predict

1. random spread between the sexes
2. bi-directional sexual transmission
3. AIDS diseases would spread from the early risk groups
4. isolation of an infectious agent

The oxidative stress theory would predict 1. non-random spread of AIDS, by exposure to oxidative risks 2. since sperm is a strong oxidative, immunosuppressive agent, the health risk from it is to the receptive anal partner, not the donor, thus no bi-directional sexual transmission. 3. AIDS diseases to remain in risk groups 4. no isolation of infectious agent (despite "Roman effort")

Comparison of predictions:
1. In the US, Western Europe, and Australia, over 80% of AIDS patients have been men since the mid 1980's. In Africa the disease affects men and women equally,
[and the symptoms are completely different].

This is paradoxical for the infectious HIV/AIDS model. In the whole history of Medicine there has never been a sexually transmitted agent/disease which is spread unidirectionally in the West and
bidirectionally (heterosexually) in Africa. A 50-50% distribution by sex vs a nearly 90-10% distribution is as different as night and day, epidemiologically.

The oxidative stress theory argues that both acquired immune deficiency (AID) and the symptoms and diseases which constitute the clinical syndrome (S) are long standing in Africa, affect both sexes equally and are caused by factors other than HIV. The presence of positive HIV serology in Africans represents no more than cross-reactivity caused by an abundance of antibodies induced by the numerous infectious and parasitic diseases which are endemic in Africa, that is, a positive HIV antibody test does not prove HIV infection. Given the above, one would expect to find a high prevalence of "AIDS" and "HIV" antibodies in Africa. This is not proof of heterosexual transmission of either HIV or AIDS. The factors uniting American AIDS patients include street drugs, hemophilia treatments, rectally deposited semen, blood transfusions, anti-AIDS pharmaceuticals including AZT, and antibiotics. It would predict AIDS would be correlated with those risk factors, and not spread randomly through both sexes by sexual transmission.

2. In 1984 Gallo and his colleagues showed that "Of eight different sexual acts, a positive HIV antibody test correlated only with receptive anal intercourse" [2]. Other data supports this conclusion[3].

It has been shown in a number of studies and should be emphasized that, unlike all sexually transmitted diseases, where both partners are equally susceptible to the disease, in homosexual males immunosuppression appears in the anal sperm recipients but not in the exclusive sperm donors.

The results seem paradoxical for the infectious model, predicted by the oxidative model.

3. In the developed world, AIDS has remained largely contained in the original risk groups.

For example, as of the beginning of 1998, 93% of the cumulative deaths from AIDS in Australia occurred in the original risk groups, that is, gay/bisexual men, drug addicts and hemophiliacs. This observation fits the classic demographic profile of non-infectious diseases which also remain confined to their risk groups.

If AIDS in Africa is the same condition with the same cause as anywhere else in the world then AIDS in Africa and AIDS in the West should be identical. This is not the case and what is called AIDS in Africa is almost unrecognizably different from AIDS in the West, so much so that if African patients suddenly switched continents, very few Africans would remain AIDS cases. This is due to the existence of multiple AIDS definitions, one for Africa (the same for adults and children), one for adults in North America, Europe and Australia, one for children in these countries and one for Latin America.

The WHO Bangui definition for Africa does not require immunological (T4 lymphocyte cell or antibody) tests or a specific disease diagnosis but consists largely of symptoms such as weight loss, diarrhea, cough and fever. For example, an African with diarrhea, fever and persistent cough for longer than one month is, by definition, an AIDS case. However, the symptoms listed in the Bangui definition (WHO, 1986) are common and non-specific manifestations of many diseases which are endemic in Africa and were so long before the AIDS era.

It is argued that the lack of spread of AIDS from the original risk groups and the fact that different risk groups have their own characteristic AIDS disease is paradoxical to the infectious model,
but not the oxidative stress model.

Even proponents of the HIV/AIDS model confirm that "AIDS does not have the characteristics of an ordinary infectious diseases. This view is incontrovertible."[Lancet 339 (1992):1289-1290] Likewise, epidemiologists Eggers and Weyer conclude that "the spread of AIDS does not behave like the spread of a disease that is caused by a single sexually transmitted agent" [Eggers, H.J. and J.J. Weyer, Linkage and Independence of AIDS Kaposi disease, Infection 19(1991):115-122.

4. Lack of isolation:
Montagnier and Gallo did use density gradient banding but for some unknown reason they did not publish any EMs of the material at 1.16 gm/ml which they and everyone afterwards call "pure HIV".

In 1997 Montagnier revealed that the reason no scanning EM's of the material that banded at the characteristic density of retroviruses was published was because even after "Roman effort", they could see no particles with "morphology typical of retroviruses".[5] He says Gallo also did not isolate.

Two historic papers in the leading science journal Virology in March 1997 disclosed "major contaminants" in "pure HIV".[6] Here is a page containing electron microsope images of the cellular debris and microvesicles which contained the proteins used to make up the antibody tests and probes and primers used in "HIV viral load" measurements

Here is a link to a photo of a proper viral isolate.

Without a proper banded viral isolate, it is impossible to say that proteins extracted from this soup of particles comes from an actual viral particle or from the contaminating cellular debris.

This is the crucial point.

If it is admitted that the majority of the material called "pure HIV" is cellular, not viral [and it is], then:

  1. How is it possible to claim proof for retroviral purification and thus for the existence of HIV?
  2. How is it possible to consider the proteins which banded at 1.16gm/ml to be the proteins of a unique retrovirus, HIV, and to use them as antigens in antibody tests to prove infection with a deadly retrovirus, HIV?
  3. How is it possible to consider the RNAs which banded at 1.16gm/ml represents the genome of a unique retrovirus and to use these as probes and primers for hybridization and PCR tests to prove infection with this virus and in fact to measure the viral load?

This is the core argument of the perth Group.

Stefan Lanka expounded on the implications of a lack of "HIV isolates" despite dogged efforts. This should not be so for a virus that exists. Lanka writes: "It has been long known that what "AIDS" researchers have presented as photos of "HIV" show normal cellular [microvesicles]... As those particles are designed, in contrast to viruses, for cellular use only, they are very unstable when removed from their context, and not able to be isolated and photographed in an isolated state. Viruses are stable because they have to leave cells or even the organism in order to infect other cells or organisms anew. Using centrifugation techniques it is no problem to separate viruses from all contaminating components and in doing so to isolate them--then photograph them, then represent their proteins and genetic substance in a direct way... Genuine viruses are so stable that it is easy... to photograph them directly as three dimensional particles in the [scanning] electron microscope without prior chemical fixation. In contrast [microvesicles] are so unstable they can only be photographed [with a transmission electron microscope, which requires they be] in a chemically fixed state... in very thin sections. All that have been shown to us as [micrographs of] "HIV" are ultrathin sections [that include what are agreed to be] cellular particles. ."

Sure enough, the micrographs of proper viral isolates presented by Lanka in his rejoinder to Steven Harris were photographed with the scanning electron microscope, and thus showed--with high resolution and three-dimensional relief--the outer surfaces of the viruses. In contrast, the purported "HIV" micrograph presented by Harris was photographed by the transmission electron microscope in "ultrathin sections," producing flat, transparent, cross-sectional images with no surfaces and poor resolution. According to Lanka, viruses are hardy enough to be photographed either way, and ought to be, since one reveals the surface in great detail, and the other reveals important cross-sectional information.

But there exists no published scanned micrograph of anything claimed to be "HIV." Since there are billions of dollars and tens of thousands of scientists annually devoted to the study of "HIV," it seems improbable that this could indicate an oversight. More likely the retrovirus-looking objects called "HIV" are, like microvesicles, simply too unstable for scanned electron microscopy and procedures that could otherwise separate them from all other objects into pure samples, which is to say-- in Lanka's opinion--they are too unstable to be viruses.

(Instability, by the way, gives the objects labeled "HIV" both the characteristics Papadopulos assigns endogenous retroviruses, the other being non-infectivity in their cell-free form.)

Wrong predictions affirm bad theories, correct predictions make them powerful.

>Each person is
>manufacturing his own endogenous retrovirus?

Either the agents to which the patients are exposed induce the right conditions or the culture conditions play a part. Perhaps a major part. The patients are sick. In fact they are sick before they ever develop AIDS. So their cells are sick and their sick cells find themselves in the right condition in cultures to be activated. That's what’s needed to produce endogenous virus and that's been known for decades.

"Normal human DNA contains retroviral information which did not get there following a retroviral infection. The cell was born with it. So amongst all our DNA there are stretches made up of some retroviral information and that may sit there maybe all your life until something happens. The DNA starts to make RNA and hence proteins, and this may go even further and lead to the assembly of endogenous retroviral particles. They're called endogenous because they're not something that got in from the outside. Like HIV is supposed to. Something that gets in from the outside is called exogenous. Long before the AIDS era everyone knew that in animal cells endogenous retrovirus production could occur spontaneously. You make a cell culture and do nothing else. Just leave it on the bench for a few days or maybe a few weeks and then one day it starts to produce retroviral-like particles. They seemingly come out of nowhere and the process can be significantly accelerated and the yield of particles increased, sometimes millions of times, by conditions which induce cellular activation, the same conditions which are obligatory to obtain what is called HIV from cell cultures. Interestingly, up until 1993, neither Gallo nor Fauci who is another well-known HIV researcher, accepted that humans contain the DNA to make endogenous retroviruses but now it's accepted that endogenous retroviral DNA forms about 1% of human DNA. For the record, that's about 3,000 times larger that what the experts claim is the size of the HIV genome. And what's more, new retroviral genomes can arise by rearrangements and recombination of existing retroviral genomes."
[Eleni Papadopulos-Eleopulos]

Having AIDS may just be a prescription for developing those abnormalities. Retrovirologists themselves have argued that retroviruses may arise as the result of a disease and not vice versa. Getting cause and effect the wrong way around is not new to Medicine.

Gallo and his colleagues serendipitously discovered a test which for some reason predicts a tendency to get sick from certain diseases that are lumped together as AIDS. But it doesn't prove that the link to all these diseases is a retrovirus.

>If there is no such thing as HIV, why would everyone's >self-manufactured retrovirus be the same?

They aren't the same. Another paradox for the infectious HIV/AIDS model, another prediction of the oxidative stress model.

In 1990 the HIV genome was said to consist of ten genes. In 1996 Montagnier reported that HIV possesses eight genes and according to Barr,-Sinoussi, HIV has nine genes. Neither is there constancy of the number of nucleotides in the "HIV genome". Thus, not only are there no two HIV genomes of the same length or nucleotide composition, there is no single genetic entity "HIV DNA" to describe the myriads of "HIV genomes". It is also estimated that patients contain between one and one hundred million distinct HIV DNAs at the one time.

How the genetic information of HIV was manufactured:

"...the majority of AIDS researchers still cling to the authenticity of HIV, because a genetic sequence for it has been published.

Since no virus has been isolated, it follows that no nucleic acid has been isolated from it either. Complicated procedures are, nonetheless, described in the literature, at the end of which something is produced which is called the nucleic acid of HIV.

  1. In a tube....

HIV and its DNA can allegedly be made by the "bucketful" but under very surprising conditions which, inter alia, entail the use of extracts from plants and other oxidizing chemicals, which could not possibly exist in vivo. Immortalized cell lines devised (and later patented) by the Montagnier and Gallo groups are co-cultured with extracts from human cells or the cells themselves. At the end of it all HIV itself is not actually obtained only reverse transcriptase activity is shown to occur which is taken to imply that the DNA that is found, must have been viral in origin.

The real explanation of what happens is as follows. In the mixture of cell cultures and stressed human cells, RNA and reverse transcriptase come to be produced in large amounts, because the cells have been specially selected and treated to do this. The RNA is transcribed into DNA by reverse transcriptase, and long pieces of DNA are produced which are said to be viral DNA. In fact they are composed of unrelated pieces of expressed cellular RNA, transcribed into DNA and linked together by a process of "template switching" (a well-characterized property of reverse transcriptase). This misleads ordinary researchers into believing that they have actually produced viral DNA. It is said that this linear DNA is the free or the non-integrated form of HIV, which furthermore is said to be a unique feature of HIV, because a lot of detectable free linear DNA has not been suggested in any other models of retroviruses.

2. Through selecting processes....

The resulting pieces of DNA too, are necessarily both shorter and longer than the "correct" length of HIV. Pieces corresponding to the "correct" length of HIV must be selected for size, because otherwise the purported DNA preparation would be a mixture of various lengths, which would violate a cardinal rule of virology that all nucleic acid of a particular virus be identical in size.

3. Through a detecting process....

Having artificially prepared DNA pieces of uniform length, they are still not ready for presentation, because they consist of a mixture of all kinds of RNA fragments transcribed into DNA and thus cannot be shown to represent unique viral DNA. Accordingly, the mixture is subjected to a kind of key-and-lock detection process called hybridization, whereby pieces of DNA are detected which complement more or less a probe of that which it is desired to be shown to have been prepared.

4. Choosing a desired probe....

Since no DNA from HIV existed to hybridize with the prepared DNA, Gallo and Montagnier simply used stretches of DNA from what they said was specific to HTLV-I, a retrovirus Gallo had earlier claimed to have discovered, and which they deemed suitable for this purpose. The DNA detected in this way was replicated and certain stretches of it cloned and declared to be the DNA of HTLV-III
(later to be called HIV).

To summarize, the purpose of the exercise is to grow HIV, but it actually produces a mixture of different lengths of DNA, contrary to theory which says they should all be identical, and no virus at all. It is then claimed that the "correct" DNA has been prepared by finding certain strands in this heterogeneous mix by hybridizing them with an HTLV-I DNA probe whose sequence is known and defined also to be HIV. However, non-hybridizing strands of DNA should not be there at all, and the fact that they are, proves that a complete rag-bag of DNA has been prepared, without any indication of what it is made up of.

It follows that "HIV" DNA must just be a laboratory artifact constructed to a preconceived idea of what retroviral DNA should be, and this assessment does not even raise the question why no virus can be obtained, whatever the experimental conditions.

One cannot help asking why no-one had not long ago spotted the flaw in the techniques employed by the Gallo and Montagnier groups. After defining some segments of DNA to be "HIV"-specific, every researcher in the field worked exclusively with short, cloned sequences (never the whole strand) on the reasonable assumption that the original characterization had been correctly performed. >From the isolation and identification procedure described above, it follows that the resultant sequences vary widely from one preparation to the next, which sequence analysts misinterpreted as the legendary capacity of HIV to mutate..."

>Why do the anti-viral drugs which arrest HIV in the test tube
>work so well on people?  Isn't this the bottom line, that mainstream
>theories of HIV infection have produced therapies which have
>greatly reduced the death rate from AIDS?

AZT has been and still remains the most recommend anti-HIV drug. Critical analysis of the presently available data which claim that AZT has anti-HIV effects shows there is neither theoretical nor experimental evidence which proves that AZT, used either alone or in combination with other drugs, has any such effect. []

HIV experts all agree that only the triphosphorylated form of AZT (AZTTP) and not the unphosphorylated form administered to patients, nor its mono- or diphosphate, is the active agent.

AZT underwent clinical trials and was introduced as a specific anti-HIV drug many years before there were any data proving that the cells of patients are able to triphosphorylate the parent compound to a level considered sufficient for its putative pharmacological action. Notwithstanding, from the evidence published since 1991 it has become apparent that no such phosphorylation takes place and thus AZT cannot possess an anti-HIV effect.

This is confirmed by the largest and most rigorous controlled study of AZT, the Concorde trial done in 1994, a double-blind randomized comparison of two policies of AZT treatment (immediate and deferred}. This involved 1749 symptom-free, HIV-infected individuals from centers in the UK, Ireland and France. The 347 clinical endpoints (AIDS and death) outnumbered the total of those in all other published trials in symptom-free and early symptomatic infection. The results showed "there was no statistically significant difference in clinical outcome between the two therapeutic policies". In 1995, extended results

of Concorde showed a significant increased risk of death among the patients treated early.
[Concorde: MRC/ANRS randomized double-blind controlled trial of
immediate and deferred zidovudine in symptom-free HIV infection. Concorde Coordinating Committee. Lancet 343:871-81.

However, despite these data, disclaimers that patients treated with AZT may continue to develop the AIDS diseases, that the side effects of AZT may mimic AIDS, and AZT given to non-HIV-infected babies causes the AIDS defining pneumonia PCP, AZT continues to be the most commonly prescribed anti-HIV drug.

A new generation of AIDS drugs, Protease Inhibitors, first became available late in 1995 and are credited with saving many lives. However, the AIDS death rate was already declining in 1994, the definition of AIDS in the US had been expanded to include people with no visible illness in 1993
[HIV/AIDS Surveillance Report, CDC. 1998.
www.cdc.g ov/nchstp/hiv_aids/stats/hasrlink.htm], and the annualized death rate of people diagnosed in 1997 was higher than in those diagnosed in 1995 and 1996. Protease inhibitors have been associated with serious health problems, including diarrhea, nausea, dangerously high cholesterol levels, diabetes and heart disease
[Carr A, Cooper DA. Gap between biology and reality in AIDS.
Lancet. 1998 Dec 19; 352(S5): 16.].

The protease inhibitors are prescribed as one of up to 200 possible "cocktails" with AZT or similar drugs. At the July 1996 XIth International AIDS conference Time Magazine Man of the Year David Ho predicted that "scientists would find new drugs to wipe HIV out of the body within three years possibly within just one".(93) At the July 1998 XIIth AIDS conference Ho stated it will take at least ten years of intense combination drug therapy to kill off all the HIV in an infected person's body but a sizable percentage of HIV patients will never get close. Many patients cannot tolerate the untoward effects of these "cocktails" and measurements show that the DNA "viral" burden does not decrease.(94-97) In the May 1998 Proceedings of the National Academy of Sciences Dr. William Paul, former Director of the National Institutes of Health's Office of AIDS Research writes, "no matter how long a person is treated with anti-HIV drugs, there will always be new viruses... you will have to be treated forever... No one is getting cured... This bodes extremely poorly for combination therapy as something curative".

Given the toxicity of these drugs, it is unlikely anyone can tolerate taking them for more than a few years. If this outlook is gloomy for HIV/AIDS sufferers, it is even worse considering there is no substantial, alternative therapeutic strategy anywhere on the horizon. The futility of all "anti-HIV" drugs, past present and future is best highlighted in a June 1998 interview by Dr. Harold Varmus, Nobel Laureate retrovirologist and Director of the NIH. "Trying to rid the body of a virus whose genome is incorporated into the host genome may be impossible". Indeed, how can a drug rid a body of material so intimately bound to the host DNA genetic material?

"The oxidative stress theory predicted that the mechanism responsible for HIV and AIDS could be prevented and treated by limiting or ceasing exposure to agents capable of inducing cellular oxidation and administering reducing agents, especially those containing sulphydryl groups (-SH) or modalities which lead to their increase, in conjunction with diet and general health care.

Although the theory has been ignored, many researchers, for reasons they have not stated, have determined the -SH levels in AIDS patients and those at risk. As the theory predicted, it was found that:

{i) The tissues of AIDS patients and those at risk, including T4 lymphocytes, are oxidized61,120.

ii) Oxidizing agents lead to the development of the phenomena which are said to prove HIV infection10,11,121.

{iii) Reducing agents cause the opposite effect; that is, they inhibit these same phenomena10,11,121.

{iv) This year, researchers from Stanford University showed that ‘GSH [reduced glutathione] levels are lower in subjects with CD4 T-cell counts below 200/ml (CD4 < 200) than in subjects at earlier stages of HIV disease; that among subjects with CD4 < 200, lower levels of GSB
[glutathione-S-bimane] (an FACS [fluorescence-activated cell sorter]
measure of GSH in CD4 T-cells) predict decreased survival; and that the probability of surviving 2-3 years increases dramatically as GSB level approach normal range. In addition, we have presented preliminary evidence suggesting that oral administration of NAC [N-acetylcysteine], which supplies the cysteine required to replenish GSH, may be associated with improved survival of subjects with very low GSH levels’120.

In other words, and as these data prove, unlike a declining CD4 cell count, there is a direct relationship between decreased cellular -SH levels and
patient survival even at CD4 cell counts < 200/mL. These data support our
theory8,10 that oxidation is of pivotal importance in the development of AIDS. Is
there not, then, a scientific justification to begin trials with -SH containing
compounds for the prevention and treatment of AIDS - especially when one considers
that some of these agents are relatively non-toxic, cheap and readily available?"

>What about the monkeys, and the SIV? Does that not exist either?

The evidence for SIV isolation and "purified" SIV is no better than that for HIV.

In addition, "SIV" does not cause any disease in wild monkeys, although roughly 50% are said to be naturally infected.

In labs, the absence of "SIV" antibodies predicted the incidence of diseases in monkeys, while the opposite is claimed for humans infected with "HIV".

In summary, I would like to say that it is not a theory to point out that "HIV" has never been isolated by the well-established guidelines:

  1. Montagnier admitted in 1997 that he did not isolate[7], and from the evidence he saw Gallo did not isolate.
  2. The Electron Micrographs of the "pure HIV" source for proteins used in antibody tests and RNAs used as probes and primers for hybridization and PCR tests to prove infection with this virus and in fact to measure the viral load reveal that the majority of the "pure HIV" is made up of cellular contaminants.
  3. Leading experts now [1997] concur[6].

"HIV" has not been isolated.

It seems improbable that this could indicate an oversight. More likely the retrovirus-looking objects called "HIV" are, like microvesicles, simply too unstable for scanned electron microscopy and procedures that could otherwise separate them from all other objects into pure samples, which is to say-- "HIV" will not be isolated.


Pat Fallon


[1] At the 1973 meeting at the Pasteur Institute the steps which
one has to follow to isolate retroviruses were thoroughly discussed and indeed are straightforward commonsense and are not dissimilar from those enumerated earlier by Beard.
1.Culture the cells that are considered infected by the retrovirus particle.
2.Purify putative retroviral-like particles by application of a method that is capable of extracting them from everything else that is not retroviral-like particles (banding in sucrose density gradients). 3. Proof obtained by use of electron microscopy that (a) there are such particles. (It is frankly misleading to proceed as if

there are particles when in fact there are none). (b)the particles are pure;
(c) the morphology of such particles is consistent with this family of viruses. Retroviral particles need to have a dense core, a diameter of 100-120 nM, to be almost spherical and to have their surface studded with knobs approximately 10nM in length.
4.Disrupt a preparation of pure particles and analyze the constituents (RNA and proteins). The latter must include an enzyme able to catalyze the synthesis of DNA from a piece of RNA.
5. Take a preparation of pure particles and prove that such particles, when introduced into fresh, uninfected cells, produce exactly the same particles, that is, the particles are infectious. This necessitates repeating steps (1) to (4). Thus proving the existence of a retrovirus involves isolating the particles twice. (And although it may seem trite to need even mention the fact, viral proteins and RNA are those and only those proteins and RNA that appear following disruption of purified viral particles).

[2]102. Goedert JJ, Sarngadharan MG, Biggar RJ, et al.
(1984). Determinants of retrovirus (HTLV-III) antibody and immunodeficiency conditions in homosexual men. Lancet 2:711-6.

In 1986 Gallo and his colleagues reported they "found no evidence that other forms of sexual activity, contribute to the risk" of HIV seroconversion in gay men.(103) In an extensive review of 25 studies of gay men reported in 1994 by Caceres and van Griensven, the authors concluded that " no or no consistent risk of the acquisition of HIV-1 infection has been reported regarding insertive intercourse".(104) In the West, the largest and most judiciously conducted prospective epidemiological studies such as the Multicenter AIDS Cohort Study (MACS) of 4955 gay men (105) have proven beyond all reasonable doubt that in gay men the only significant sexual act related to becoming HIV antibody positive is receptive anal intercourse. Thus in gay men, AIDS may be likened to the non-infectious condition, pregnancy. It is acquired by the passive partner but is not transmitted to the active partner.

Significantly, the MACS also showed that once a gay man becomes HIV positive, progression to AIDS is further determined by the amount of passive anal intercourse sustained after "infection". This is contrary to all that is known about infectious diseases. Infection, not repeated infections, causes disease.

The largest and best conducted studies in heterosexuals including the European Study Group (107) show that for women, the only sexual practice leading to an increased risk of becoming HIV antibody positive is anal intercourse. The unidirectional transmission of "HIV" observed in OECD countries is supported by Nancy Padian's ten year study of heterosexual couples (1986-1996).(108)

[4][Coombs RW, Welles SL, Hooper C, et al. (1996). Association
of plasma human immunodeficiency virus type 1 RNA level with risk of clinical progression in patients with advanced infection. AIDS Clinical Trials Group (ACTG)116B/117 Study Team. ACTG Virology Committee Resistance and HIV-1 RNA Working Groups. J. Infect. Dis., 174, 704-712.

[5][Tahi D. (1998). Did Luc Montagnier discover HIV?
Text of video interview with Professor Luc Montagnier at the Pasteur Institute July 18th 1997. Continuum 5:30-34]

[6]Bess JW, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO. (1997).
Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virol. 230:134-144.

Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. (1997). Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virol. 230:125-133.

[7]On July 17th 1997, the French investigative television journalist
Djamel Tahi interviewed Professor Luc Montagnier in camera at the Pasteur Institute in Paris. Montagnier was asked, "Why do the EM photographs published by you [in 1983] come from the culture and not the purification?". His reply was, "There was so little production of virus it was impossible to see what might be in a concentrate of the virus from the gradient ["pure virus"]. There was not enough virus to do that. Of course one looked for it, one looked for it in the tissues at the start, likewise the biopsy. We saw some particles but they did not have the morphology typical of retroviruses. They were very different.Relatively different. So with the [unpurified] cultures it took many
hours to find the first pictures. It was a Roman effort!… Charles Dauget
[an EM

expert] looked at the plasma, the concentrate, etc… he saw nothing major".
Questioned about the Gallo group he replied, "Gallo? I don’t know if he really purified. I don’t believe so". This should have been both the beginning and the end of HIV.