Questions and Answers 13 October 2003
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Eleni Papadopulos-Eleopulos,
Biophysicist
Department of Medical Engineering and Physics, Royal Perth Hospital, Western Australia 6847,
Valendar F. Turner, John Papadimitriou, Barry A. P. Page, David A. Causer, Helman Alfonso

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Re: Questions and Answers

In his rapid response "Re: The Perth Group answer to Christopher Noble" (5th September 2003), Brian Foley wrote: "The Perth group wrote "While the present dissimilarities in the "HIV-1" genome appeared at the time of its transmission to humans (a few decades ago), the present dissimilarities in the HPV types existed since the ancient times. While the "HPV genotypes are quite stable over both time and space", there is "an extraordinary scale of HIV variation" both in time and space (5). "

This is not correct. The diversity in HIV-1 M group sequences did not spontaneously appear at the the time of the alleged transmission from chimpanzee to humans. It accumulated over time since the transmission. Likewise, the diversity in the HPVs (which evolve at a rate at least a hundred thousand-fold slower than retroviruses) did not exist since ancient times, it has accumulated over time.

What point is the Perth group trying to make? Yes, lentiviruses are retroviruses with error-prone replication, so they evolve faster than DNA viruses. Is that supposed to prove that they can't exist? "

Where is the proof that "HIV" was transmitted from chimpanzee to humans?

Where is the proof that the diversity in HIV-1 M group sequences have accumulated over time since the transmission?

Even in the first sequencing of the "HIV" genome, Gallo and his colleagues reported "polymorphism in the coding regions of the genome…" (1)

The diversity of the "HIV" genome led researchers from the Pasteur Institute as far back as 1989 and 1992 to conclude: "The task of defining HIV infection in molecular terms will be difficult" (2,3)

The "point" that we are making is not what Brian Foley implies. The "point" we want to make is: we would like someone to show us how it is possible that given the "extraordinary scale of HIV variation" (4) to have proteins which have the same function, to induce the same antibodies which can be detected with a single antibody test, and to define "HIV" infection in molecular terms.

Brian Foley wrote: "The Perth group wrote: "While "HIV-1" (all groups) is said to always cause a fatal syndrome, AIDS, in all infected individuals, only "a small fraction" of the HPV types are associated with "disease burden"."

Again they are mistaken. No virus (with the near exception of some strains of rabies virus) ever kills 100% of the hosts that it infects. Nobody has ever presented any scientific evidence that HIV-1 can or does kill all infected people. It may be true that somebody said this, but it is not a true statement.

We never said that a virus "kills 100% of the hosts that it infects" much less "HIV-1". However, many people not only "somebody" have made this claim for "HIV". We made mention that it is understood that the genomic variability in the HPV types renders them either being or not being associated with disease. The point that we want to make is for someone to show us how it is possible that given the "extraordinary scale of HIV variation" (4) for all of the "HIV" groups to be associated with AIDS.

The HIV-1 M group of viruses and the HIV-1 O group of viruses are not "one and the same thing". Calling them "one and the same thing" just because they have been named "HIV-1" and because they infect CD4+ T-cells of primates and cause AIDS in humans, is analogous to calling mice, elephants and cats "one and the same thing" because they have been named "mammals" and because they produce live young , feed them milk and breath air.

The HIV-1 M, N and O groups of viruses do have some things in common, just as all mammals do, but they also have many important differences. "

Our understanding is that the genomic differences in mammals cause them to have different phenotypes and functions. For example, "mice, elephants and cats" all look different and behave differently. Would Brian Foley tell us what are the differences (apart from genomic differences) between the "HIV-1" groups? We note that these groups are all labelled "HIV-1" which stands for human immunodeficiency virus, not viruses unlike "mammals" which is obviously plural and includes all individual varieties.

Brian Foley wrote: "The perth group wrote: "So we again ask if Brian Foley would provide us with references which prove that the "HIV" sequences originated from a unique infectious retroviral particle, HIV."

What part of "infectious molecular clone" do you fail to understand? We have been over this a few times before, already. If you have a segment of DNA that produces infectious viral particles it is clear that this segment of DNA contains a viral genome."

We wrote "a unique infectious retroviral particle", not an "infectious molecular clone". Yes, we "have been over this a few times before, already." Brian Foley has never answered us. For example, where is the evidence that "a segment of DNA that produces infectious viral particles"?

Brian Foley wrote: "When the segment of DNA is sequenced and found to contain Gag, Pol and Env genes it is extremely clear that the viral genome is a retroviral genome."

Gag stands for group specific antigens. Pol stands for polymerase proteins. Env stands for envelope proteins. Where is the proof that the "HIV" Gag, Pol and Env proteins are coded by the "HIV" Gag, Pol and Env genes?

Brian Foley wrote: " If there was any question about this, then DNA evidence could never be used in courts of law; the blood stains found at a crime scene could be beef blood from a steak that was cut up. You don't have to "isolate" a human in order to tell whether the blood came from a human, you only need to sequence it."

The only reason that we know the blood came from a human is because the first people who did the sequencing were 100% sure that the blood came from humans and not from the abattoir. This is not the case with the first "HIV" genome. As we have already pointed out to Brian Foley in our previous rapid response "HIV Genome, Clones and Sequences" (18 July 2003), what Montagnier’s and Gallo’s groups defined as "HIV" genome is nothing more than a poly(A)-RNA which in sucrose density gradients banded at the 1.16gm/ml. They claimed that the band represented "purified" virus but presented no EM proof. According to Montagnier the reason for this is because in the "purified" virus they could find no particles with the morphology typical of retroviruses.(5)

As we repeatedly pointed out the only electron micrographs published to date are those of Bess et al (6) and Gluschankof (7). Although they spared no effort their "purified" HIV consisted mainly of cellular fragments and some particles which they called "HIV" but not one of which had all the morphological characteristics attributed to it. In other words, the "HIV" genome may have come from anything which bands at 1.16gm/ml but not from a retrovirus particle much less a unique retrovirus, "HIV".

Would Brian Foley please answer the following question: Isn’t it true that this is how the "HIV" genome was obtained? If not, would Brian Foley please tell us where we are wrong?

As far as the use of DNA evidence in court is concerned, for the sake of argument let us assume that particles with the morphological characteristics of Lentiviruses have been purified from cell cultures derived from AIDS patients. That is, the particles have been separated from all other material which is not retroviral particles. If a scientist were to obtain the RNA from this material would Brian Foley agree such RNA is that of the retrovirus? If he agrees can he produce the evidence such an experiment has been performed? If he is not able to produce such evidence yet asserts the "HIV" genome is nonetheless bona fide, then we must conclude Brian Foley knows another method for proving the same thing which does not involve purification. Whatever this method may be, it must distinguish between RNA which is retroviral and RNA which is not. If we ask Brian Foley to describe this method then, unless he has performed unpublished experiments of his own, he can only refer to published data. So far Brian Foley has not given us such a method.

In case other readers of this BMJ Online debate think there is something "magical" about the methods of molecular biology, let us explain why we think as we do. It is a fundamental fact that in everyday medical practice ultimate proof of ownership of organs, tissues, blood or other biological material relies entirely on documenting their removal from the body of a unique member of the species Homo sapiens. If a surgeon removes a patient’s appendix, several witnesses observe it taken from the abdominal cavity of a person identified by a name band and medical record number. The specimen is then placed in a bottle of formalin bearing a label with the same name and unique number. Thus medical practice abounds with forensic precautions for designating and preserving the identity of such specimens as they pass from patient to laboratory for processing. Plainly put, both doctor and Mrs Jones are interested solely in the result of Mrs Jones’ pregnancy test. Not Mrs Brown's. The same rigour is demanded by courts of law when it comes to admissibility of evidence in regard to blood alcohol readings or DNA analysis. Likewise, proof that particular biochemical entities are viral demands the same standard of proof, that is, the principle we may call virological habeas corpus.

Brian Foley wrote: "The Perth group is being blatantly dishonest to claim that they are the world's authority on virology, epidemiology and genetics and that if their impossible rules are not followed then the virus might not exist."

We never claimed to be "the world’s authority on virology, epidemiology and genetics". We are scientists and science is all about questions and experimental proof. For example, when somebody like Christopher Noble says: "these two subtypes of hemagglutinin from influenza A, isolated from humans at approximately the same time, differ from each other by 81% at the amino acid level." but do not explain how it is possible that two viral particles having proteins which vary by 81% are one and the same virus and the proteins perform the same functions;

or like Montagnier "That this new isolate was a retrovirus was further indicated by its density in a sucrose gradient which was 1.16…" and that the 1.16gm/ml band was "purified labeled virus"(8) and then he says that in the 1.16gm/ml band, he could not find any particle with the morphology typical of retroviruses (5);

scientists would ask the question what is going on here?

When someone like Montagnier says "analysis of the proteins of the virus demands mass production and purification." (5) and that he characterised the "HIV" proteins in this manner (6) and then he says "I repeat, we did not purify" (5);

Or like Gallo "Montagnier subsequently published many EM pictures of purified HIV particles, as, of course, we did in our first papers. You have no need to wrory. The evidence is obvious and overwhelming." (9) but nowhere in the scientific literature are there any EM pictures of "purified HIV particles" published by anybody including Montagnier and Gallo anywhere even in Gallo’s first papers;

You don’t have to be even a scientist to ask the question what is going on here?

It is commonsense that if you claim that X is a constituent of Y, you must have proof that X originated from Y. In this regard, one must have proof that the fragment of RNA which is said to be the "HIV" genome originated from "HIV" particles. We have been looking for this proof for 19 years and so far we have not been successful. We asked virologists including Brian Foley and Christopher Noble for references containing evidence for such proof. So far no references have been forthcoming. Therefore, again the question needs to be asked what is going on?

When the two most important predictions of the "HIV" theory of AIDS were: (i) that the cause of KS is "HIV", (in fact KS was the main basis for the retroviral theory of AIDS.) but today everyone accepts that "HIV" is not the cause of KS; (ii) that although initially "HIV" was restricted to the risk groups (gay men, IV drug users, haemophiliacs), it would rapidly spread through the general population via sexual intercourse, but in the developed world, "HIV" is still restricted to the risk groups (this could not be due to sex education because sex education was introduced in the second half of the 1980s by which time "HIV" infection had peaked in gay/bisexual men and haemophiliacs and also no amount of sex education has any effect on "HIV" transmission not even in Africa (10));

then given that a theory is as good as its predictions, any scientist would ask the question what is going on here?

Brian Foley wrote: "No virus has ever been "isolated" and studied in such a way as to meet all of the Perth group's requirements. In fact the Perth group knows that lentiviruses are asymetrical and that is why they keep parroting the requirement that preparations of the virus must show that "No apparent differences in physical appearance could be discerned". It has always been clear that electron micrographs of all lentiviruses show differences because some of the virion particles are viewed end-on and some are viewed from the side in any micrograph."

Let us repeat that these are not requirements that we formulated. They are requirements set down by Barre-Sinoussi and Chermann, the principal and second author of the 1983 Science paper where it is claimed the existence of "HIV" has been proven.

It is unclear what Brian Foley means by "asymetrical". Does he refer to the particle or its contents?

Brian Foley wrote: "The Perth group writes: "...we have been asking for help and are willing to be educated. "

When in fact they have been repeatedly informed that their criteria for isolation/purification of retroviruses are not valid, and have never been carried out on any virus. They do not present themselves as students, willing to learn about virology and epidemiology, but as "experts" who join with others to advise the government of South Africa not just to study HIV research, but to declare HIV research completely invalid until their impossible rules for isolation/purification have been met.

They do not claim that they are ignorant of virology and ask virologists to explain how it is, exactly, that we study viruses using molecular biological techniques. Instead they claim that they have the only valid technique and until all of their conditions are met the virus has not been "proven" to exist."

Once again let us repeat that the criteria for isolation/purification but are those of some of the most imminent retrovirologists including Gallo and Montagnier. In fact this is exactly the method used to prove the existence of "HIV" but for reasons which became clear later they did not publish electron micrographs of the "purified virus".

Yes, we "willing to be educated" with scientific facts and not to be told just to believe and not "to wrory. The evidence is obvious and overwhelming".

Brian Foley wrote: "They then go on to claim that until the virus is proven to exist by their exact criteria and methods, that no other tests such as serological tests or molecular biology can be used to study the virus."

Yes, unless you prove the existence of "HIV", you cannot do serological tests or molecular biology studies of "HIV". To perform "HIV" serological studies, you need "HIV" proteins. Gallo considers p41 to be the most important "HIV" protein (11), whereas Montagnier considers p24 to be the most important "HIV" protein (8). According to Montagnier: "analysis of the proteins of the virus demands mass production and purification." (5). (Of course this is also true for the "HIV" genome.) However, as he already admitted, the "HIV" p24 protein originated from the 1.16gm/ml band where he did not even have particles with the morphology of retroviruses. This means that the p24 protein could not be "HIV" or even retroviral. Furthermore, unlike Gallo, Montagnier considers p41 to be the ubiquitous cellular protein actin. (5,8)

Of course, serological tests can be done and like the ESR may be useful in clinical practice (12) but it doesn’t mean that they prove "HIV" infection. This is a fact accepted by the manufacturers of the test kits: "At present there is no recognized standard for establishing the presence or absence of antibodies to HIV-1 and HIV-2 in human blood" (13)

Since like for the protein there is no proof that the "HIV" genome originated from "HIV" particles there can be no molecular biological studies of "HIV".

One test manufacturer of the "HIV" PCR kits states: "AMPLICOR HIV-1 MONITOR Test is not intended to be used as a screening test for HIV or as a diagnostic test to confirm the presence of HIV infection" (Roche Diagnostic Systems AMPLICOR HIV-1 MONITOR Test package insert, PMA No. BP950005/4).

In the CDC 2000 Revised AIDS Surveillance Definition, it is stated: "In adults, adolescents and children infected by other than perinatal exposure, plasma viral RNA nucleic acid tests should NOT be used in lieu of licensed HIV screening tests (e.g. repeatedly routine enzyme immunoassay)" (emphasis in original). The question is how one and the same test for one and the same virus can "NOT" be used to prove infection in adults, adolescents and in children infected by means other than mother-to-child transmission — but can be used to prove the latter.

Brian Foley wrote: "In response to my observation that the relative purity of HIV-1 viral particles ranged from low to high in the Bess paper: {Virology 230(1):134-144 (1997)}, The Perth group writes: "In addition, the CEM-SS cells contains low amounts of â2-M proteins and Implicitly, microvesicles purified from cell lines such as CEM-SS and MOLT-3 that do not produce HLA-DR did not contain any HLA-DR. (1) This fact alone will result in a high ratio even if the purity is extremely low. "

This is a clever attempt to mislead readers into thinking that the ratio I remarked on, of 150:1 or more than 99% "purity" might have been from one of these cell lines that do not produce HLA DR. I encourage anyone who wants to know more to read the Bess paper itself, and not trust the Perth group's "spin" on what it says."

For those readers who may have difficulty in accessing the Bess paper, here are the sections of the Bess paper relating to the 150:1 ratio:

"Implicitly, microvesicles purified from cell lines such as CEM-SS and MOLT-3 that do not produce HLA-DR did not contain any HLA-DR but did contain β2-M…As seen in table 1…The HIV-1(MN) Clone 4-infected CEM-SS, DAUDI, and MOLT-3 cells also provided good virus yields.”

TABLE 1

Analysis of HIV-1 or Microvesicles Recovered from Various Cell Lines
 
                  HIV-1                         HIV-1
Cell Line  Lowry  p24CA RIA  HLA DR    b2-M RIA p24CA to
           mg/ml    ng/ml    RIA ng/ml   ng/ml  HLA ratio

HIV-1(B)/H9              4.40  11,216  50,540 8,366  0.19:1 
HIV-1(MN)/H9             7.84   2,426 113,147 1,542  0.02:1 
HIV-1(MN)/H9 Clone 4     4.04 208,348  38,618 6,566  4.61:1 
HIV-1(MN) Clone 4/CEM-SS 3.73 125,096       0   830 150:1 
HIV-1(MN) Clone 4/DAUDI  6.41  87,154     734     0 119:1 
HIV-1(MN) Clone 4/MOLT-3 1.99  25,734       0 3,205  8.03:1 
H9                       3.83       0  29,832 4,558  N/A 
CEM-SS                   1.49       0       0   519  N/A 
DAUDI                    2.82       0     787     0  N/A 
MOLT-3                   1.87       0       0  1960  N/A
 

 

Brian Foley wrote: "If you visit the Perth group website at: http://www.theperthgroup.com/aids/

you find that they are not presenting data, such as interviews with dozens of AIDS patients who all claim they could not have been infected with a virus, or data showing that the epidemiology of AIDS fits with their theory that AIDS cannot be sexually transmitted and is due instead to "oxidative stress". Instead you find their clever rhetoric, mostly based on the idea that if the virus has not been isolated/purified by their exact criteria then all other research on HIV and SIV is invalid."

What Brian Foley is suggesting is a study of patients who "claim they could not have been infected with a virus". Presumably Brian means patients who are HIV seropositive but who claim they could not have been infected with HIV. If there were such a study how would it alter matters? All HIV experts and Brian Foley accept the antibody tests as being highly specific for HIV infection. Thus, regardless of how a person may know whether or not a viral infection could have taken place, all such individuals are infected. If Brian Foley can name one expert who thinks otherwise then he should ask that expert why he has not published a paper expressing doubts about the specificity of "HIV" serology. As we have done over many years and for many more reasons than the handful of patients who have approached us because of the conviction they could not have been infected with HIV.

We have repeatedly presented evidence including in this debate and journal (14) that at present there is no proof of "HIV" sexual transmission. The fact that we repeatedly have asked for studies with such proof and neither Brian Foley nor anybody else has given such references suggests that we may be right. (In his rapid response "Re: Re: A critical examination of the evidence for the existence of HIV" (20th September 2003), Brian Foley wrote: "that AIDS was caused by a microorganism that could pass through a submicron filter, and be transmitted sexually and via blood products but not via casual contact was clearly reached by mid 1982 and has been reconfirmed over and over again since then." However, in not one of the many references that he gives to support his claim does such proof exist.) It follows then that either AIDS is not sexually transmitted and its cause may be oxidative stress or that AIDS is sexually transmitted but its cause is not "HIV".

Indeed, "if the virus has not been isolated/purified", that is, its existence has not been proven then it cannot be claimed to be the cause of AIDS.

Brian Foley wrote:" For example, in their slide show and accompanying text: The Perth Group presentation to the Presidential HIV/AIDS Panel Johannesberg 3rd and 4th of July 2000 (Powerpoint file) and Text of The Perth Group presentation to the Presidential HIV/AIDS Panel Johannesberg 3rd and 4th of July 2000 They state this about the figure 1 of the Bess paper: "The infected cultures originate from AIDS patients who are highly oxidised and these cultures are chemically stimulated."

In fact, the MN isolate of HIV-1 subtype B used by Bess et al. was isolated in 1984 from a young boy. Does the Perth group have information about how this boy became "highly oxidised", and how that oxidised property is able to be passed from culture to culture and even re-cloned?"

In the Bess paper, one reads "HIV-1(MN) infected H9 cells [HIV(MN)/H9] (Reitz et al, 1992)". The 1992 Reitz, Gallo et al paper is entitled "On the Historical Origins of HIV-1 (MN) and (RF)". In regard to "HIV-1(MN)" they wrote: "The patient from whom the MN virus was obtained was a pediatric AIDS patient from the Newark, NJ area. He was first seen at St, Michael's Medical Center at age 3 in October 1983 for management of low platelet counts and epistaxis which had begun in April 1983. Some lymphadenopathy was noted. His mother was an IV drug user, who died of pneumonia in 1982. A blood sample was sent to the Laboratory of Tumor Cell Biology (LTCB), NCI, NIH, in February 1984 and cocultivated with cord blood lymphocytes. The culture was positive for reverse transcriptase in early March 1984. This was one of the positive cultures reported by Gallo et al5, but it was not identified by name. Both the patient and his father were found to be seropositive for HIV-1. HIV-1(MN) was successfully transmitted [reverse transcription was detected] first to the H4 and then the H9 clonal derivatives of HUT-787 as described in Popovic et al6. The resultant cultures were designated PH-1 and continuously produced HIV-1(MN) [continuos detection of reverse transcription]. This is the source of the MN virus which has been used by laboratories around the world."

Note that the only proof which Gallo had given for "the MN isolate" and its transmission and thus for the existence "of the MN virus which has been used by laboratories around the world" is detection in cultures of reverse transcriptase activity (RT), which is non-specific to retroviruses.

One of the main predictions of the oxidative theory of AIDS was that AIDS patients and those at risk would be oxidised, a prediction which has been fulfilled beyond reasonable doubt. In fact, oxidative stress is a better predictor of the development of AIDS than the T4 cell numbers.(15) Since "this boy" had AIDS, it is expected that he would be oxidised. In addition, "His mother was an IV drug user" (the drugs are oxidising agents). Since the drugs would have crossed the placenta, both the mother and the boy would be oxidised. In reference 5 of the Reitz, Gallo et al paper, which is one of the four 1984 papers by the Gallo team, the cultures were stimulated with two oxidising agents, "T-cell growth factor (TCGF)" and "phytohemagglutinin (PHA-P…)".

The H4 and the H9 HUT-78 clones to which "HIV-1(MN) was successfully transmitted…as described in Popovic et al" were obtained by "using irradiated mononuclear cells from peripheral blood of a healthy donor as a feeder", that is, by culturing them with oxidised cells.(16)

In the Bess paper, it is stated that "HIV-1(MN)/H9 Clone 4 was prepared by Dr. Steve Nigida (AVP) and is a single-cell clone of HIV-1(MN)/H9 prepared by limiting dilution (Ott et al, 1995a)." In the Ott et al paper, one reads: "The cell cloning of the H9 cell lines was accomplished by plating HIV-1 (MN)-infected cells from our stock culture into 96-well plates at an average cell density of 0.05 cell per well along with mitomycin (Sigma, St Louis, Mo)-treated H9 feeder cells at 2 x 105 cells per well. For the subcloning of Clone 4, we used gamma-irradiated (cumulative dose, 5,000 rads) BS-C-1 African green monkey kidney cells as feeder cells at 1.6 x 104 cells per well." (15) That is, "Clone 4" was obtained by further oxidation of the cell cultures.

Since "HIV-1(MN)" has been used by laboratories around the world included Bess’ laboratory, in his view would Brian Foley please tell us which of Gallo’s evidence proves the existence of "HIV-1(MN)"?

References

1. Ratner L, Haseltine W, Patarca R, Livak KJ, Starcich B, Josephs SF, Doran ER, Rafalski JA, Whitehorn EA, Baumeister K, Gallo RC, Wong-Staal, F. (1985) Complete nucleotide sequence of the AIDS virus, HTLV-III. Nature 313: 277-284

2. Vartanian JP, Meyerhans A, Henry M, Wain-Hobson S. (1992) High-resolution structure of an HIV-1 quasispecies: identification of novel coding sequences. AIDS 6(10): 1095-1098.

3. Meyerhans A, Cheynier R, Albert J, Seth M, Kwok S, Sninsky J, et al. (1989) Temporal fluctuations in HIV quasispecies in vivo are not reflected by sequential HIV isolations. Cell 58(5): 901-910.

4. Korber B, Gaschen B, Yusim K, Thakallapally R, Kesmir C, Detours V. (2001). Evolutionary and immunological implications of contemporary HIV-1 variation. British Medical Bulletin 58: 19-42.

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

7. 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. Virology 230: 125-133.

8. Barre-Sinoussi F, Chermann JC, Rey F, Nugeyre MT, Chamaret S, Gruest J, Dauguet C, Axler-Blin C, Vezinet-Brun F, Rouzioun C, Rozenbaum W, Montagnier L (1983) Isolation of a T-Lymphotrophic Retrovirus from a patient at Risk for Acquired Immune Deficiency Syndrome (AIDS). Science 220: 868-871.

9. Gallo RC (2003) Email communication with VF Turner.

10. Kamali A, Quigley M, Nakiyingi J, Kinsman J, Kengeya-Kayondo J, Gopal R, Ojwiya A, Hughes P, Carpenter LM, Whitworth J. (2003) Syndromic management of sexually -transmitted infections and behaviour change interventions on transmission of HIV- 1 in rural Uganda: a community randomized trial. Lancet 361: 645-652

11. Schupbach J, Popovic M, Gilden RV, Gonda MA, Sarngadharan MG, Gallo RC. (1984). Serological analysis of a Subgroup of Human T-Lymphotrophic Retroviruses (HTLV-III) Associated with AIDS. Science 224: 503-505.

12. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Alfonso H, Page BAP, Causer D, et al. (2003) High rates of HIV seropositivity in Africa-alternative explanation. International Journal of STD and AIDS 14: 426-430.

13. Packet Insert Axsym system (HIV-1/HIV-2). Abbott Laboratories Diagnostics Division. 100 Abbott Park Rd. Abbott Park. Illinois: United States of America. 1988, 1998. http://aids-kritik.de/aids/diverses/abbott-hiv-test.htm

14. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Alfonso H, Page BA, Causer D, et al. (2002) Global voices on HIV/AIDS. Heterosexual transmission of HIV in Africa is no higher than anywhere else. British Medical Journal 324: 1035

15. Herzenberg LA, De Rosa SC, Dubs JG, Roederer M, Anderson MT, Ela SW, Deresinski SC. (1997) Glutathione deficiency is associated with impaired survival in HIV disease. Proc. Natl. Acad. Sci. USA. 94: 1967-1972.

16. Popovic M, Sarngadharan MG, Read E, Gallo RC. (1984). Detection, Isolation, and Continuous Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 224: 497-500.

Competing interests:   None declared