HIV in South Africa 13 March 2003
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Eleni Papadopulos-Eleopulos,
Medical Physicist
Perth Western Australia 6009,
Valendar F. Turner, John M Papadimitriou, Barry A. P. Page, Sam Mhlongo, Helman Alfonso, David Causer, Christian Fiala and Anthony Brink

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Re: HIV in South Africa

HIV in South Africa


We agree with Fassin and Schneider (Education and Debate, 1 March) that “contrary points of view should be understood rather than discredited”.  Consider their statement “…denial – a common response among people facing an intolerable situation – has two facets.  One is a denial of reality: a reaction that something can’t be true, that it is not possible.  The other is a denial of the unacceptable: a reaction that something is not normal, that although it exists it should not.  Both facets are involved in the denial of the reality of HIV/AIDS.”  Nobody denies that an epidemic of poverty and disease exists in South Africa and they go hand-in-hand.  The “controversies” are: Is the disease caused by a retrovirus and is it sexually transmitted?


Sexual Transmission of HIV

In the first study conducted in gay men to examine the relationship between AIDS and sexual activity (before HIV was accepted as the cause of AIDS), the authors reported “…the number of partners per month in receptive anal-genital intercourse with ejaculation, the number of occasions of “fisting”,…were the only independent and statistically significant variables for discriminating patients from controls”.1  In 1984, Robert Gallo and his colleagues wrote “Of eight different sex acts, seropositivity correlated only with receptive anal intercourse…and with manual stimulation of the subject’s rectum (receptive “fisting”)…and was inversely correlated with insertive anal intercourse.”2  Two years later they confirmed their 1984 findings: “In this analysis, only receptive rectal intercourse, douching, rectal bleeding…were significant predictors (p<.05) of anti-HTLV-III positivity…We found no evidence that other forms of sexual activity contributed to the risk.”3  In a 1994 review of all the major studies conducted in gay men including the longest, largest, best-designed and executed published study of gay men anywhere in the world, the MultiCenter AIDS Cohort Study, the authors concluded:

“(1) unprotected anogenital receptive intercourse poses the highest risk for the sexual acquisition of HIV-1 infection;  (2) anogenital insertive intercourse poses the highest risk for the sexual transmission of HIV-1 infection;  (3) there is mounting epidemiologic evidence for a small risk attached to orogenital receptive sex,…(4) sexual practices involving the rectum and the presence of (ulcerative) STD facilitate the acquisition of HIV-1;  (5) no or no consistent risk for the acquisition of HIV-1 infection has been reported regarding other sexual practices such as anogenital insertive intercourse and oroanal sex…”.4


Since the main and absolutely necessary property of sexually transmitted agents is bidirectionality, that is, transmission from the passive to the active partner and vice versa, this means HIV cannot be sexually transmitted.


One of the first case reports of heterosexual transmission was published by Luc Montagnier and his associates in 1985.  The wife of an HIV positive haemophiliac who practised vaginal, oral and anal intercourse was found to be seropositive and to have low T4 cells.  She was followed for ten months after exposure to her husband’s semen was discontinued.  When retested her T4 cells were normal and had a negative antibody test.5   In one of the largest prospective studies conducted in HIV positive haemophiliacs and their spouses, no women seroconverted.  The authors “calculated that in 11 couples unprotected vaginal intercourse occurred a maximum of 2,250 times (minimum 1,563) without transmission of HIV”.6  In a similar study, the authors concluded “The most likely value of the probability of infection within 25.8 months for this group of 36 sexual partners is zero…The absence of seropositivity in any of the 36 sexual partners included in this study indicates that heterosexual transmission in this group with no additional risk factor is uncommon."7  The Padian et al study (the longest, largest, best-designed and executed published study of heterosexuals anywhere in the world) consisted of two parts, a cross-sectional and a prospective.  In the prospective study, despite the fact that even at the end of the study 25% of the couples were not “consistently” using condoms, no HIV transmission was reported.  In the cross-sectional part, in 10 years they reported only two cases of female-to-male transmission, but the authenticity of both was questioned by the authors themselves.  There were more cases of male-to-female transmission and in these cases “Anal intercourse significantly discriminated between seronegative and seropositive women”;8 “…only the practice of anal intercourse (p = .003) and non-white race (p = .015) were significantly associated with infection”.9  In the largest European study (9 centres from 6 countries) “The only sexual practice that clearly increased the risk of male-to-female transmission was anal intercourse…no other sexual practice has been associated with the risk of transmission”.10


In the most recent analysis of heterosexual transmission, the authors wrote: “Though heterosexual intercourse has been virtually the sole explanation offered for the AIDS epidemic in sub-Saharan Africa, to our knowledge in no other part of the world has penile-vaginal exposure (as opposed to ‘heterosexual sex’) been demonstrated to initiate or sustain rapid HIV propagation.  HIV is not transmitted by ‘sex’, but only by specific risky practices…Dispassionate assessment of our conclusions admittedly depends on a willing suspension of disbelief, since the current paradigm is deeply embedded”.11  Last year in this journal we presented evidence that in Africa there is no more heterosexual transmission than anywhere else in the world.12  One of the most eminent HIV experts, Jaap Goudsmit, acknowledges that for heterosexual HIV transmission “…a homosexual or anal factor seems to be required…Studies in Thailand showed that even frequency of intercourse did not promote the transmission of HIV-1B, as long as the intercourse was vaginal not anal…Limited studies of heterosexual couples in Africa suggest a parallel…”.13


In conclusion at present there is ample epidemiological evidence which shows that:

(a)   The only sexual act, in both gay and heterosexual sex, which is related to the appearance of AIDS and a positive antibody test is receptive anal intercourse.

(b)   It is not homosexuality per se but the sexual act (“anal intercourse may be practiced by a much larger absolute population of heterosexuals than of homosexuals”14) which is important.  Thus, like pregnancy, AIDS and a positive antibody test can be sexually acquired but not sexually transmitted.  The difference is that while pregnancy can be acquired by a single act of sexual intercourse, for AIDS to appear a very high frequency of receptive anal intercourse over a long period is necessary.12


HIV Antibody Tests

The only test routinely used to prove HIV infection is the antibody test.  In clinical practice such a test cannot be used unless it is first proven specific.  In the HIV antibody test literature it is claimed that the tests are either 100% specific or they approach this accuracy.  The same literature also shows that the specificity has been determined by: comparing one antibody test with another;  testing known positive and negative samples;  testing young healthy blood donors.  Basic scientific methods rule out specificity being determined in this manner.  Only comparing the reactivity with the presence or absence of HIV will determine the specificity of the antibody tests.  That is, HIV isolation/purification must be used as the gold standard for the antibody tests.  However, at present some of the best known HIV/AIDS experts agree there is no such gold standard.  "One difficulty in assaying the specificity and sensitivity of human retroviruses [including HIV] is the absence of a final 'gold standard'".15 16  According to one antibody test manufacturer “At present there is no recognized standard for establishing the presence or absence of antibodies to HIV-1 and HIV-2 in human blood…Specificity based on an assumed zero prevalence of antibody to HIV-1 and/or HIV-2 in random donors…is estimated to be 99.90%…”.17  The specificity of the Western Blot (WB), the test which is used as a gold standard for all the other antibody tests as well as for the PCR test,18 19 cannot be determined even if a gold standard exists.  This is because the WB is not standardised20 21  (see ).  It follows that the specificity may be anywhere between 0% and 100%.


In the vast majority of studies conducted in Africa the authors do not even follow the algorithms recommended by the manufacturers. One example is the latest and largest study conducted in South Africa and said to have shown that “South Africa has the highest number of people with HIV in the world”, “five million people infected”.  The manufacturer of the test used in this study points out that the test cannot be used to prove HIV infection but only as a screening test to be confirmed by WB.  Furthermore, the “OraSure® HIV-1 Oral Specimen Collection Device is intended for use in the collection of oral fluid specimens for testing for antibodies to the Human Immunodeficiency Virus-Type 1 (HIV-1) in subjects 13 years of age and older”.22 23  Yet the test (a single ELISA without a confirmatory test) was used to test all individuals including children aged between 2 and 13 years and the results were interpreted as proving that 11.4% of South Africans are HIV infected.24


In addition, the antigens used in the antibody tests may not even be HIV proteins.  According the discoverer of HIV, Luc Montagnier, to characterise the HIV proteins the virus must be purified.  Although in 1983 he and his group claimed to have done so and to have obtained the HIV proteins from the “purified” virus, in 1997 he admitted that even after "Roman effort", in electron micrographs of their "purified" virus they could not see any particles with the "morphology typical of retroviruses.”25  This means that the “HIV” proteins could not have been those of a retrovirus, HIV.  By 1997 some of the best known HIV experts pointed out that HIV “used for biochemical and serological analyses or as immunogens is frequently prepared by centrifugation through sucrose gradients", but in none of the studies "the purity of the virus preparation has been verified".26 27  In other words, up till 1997 nobody had published electron micrographic proof that the "purified virus" contained nothing else but isolated retroviral particles.  In that year two studies were published, one by a US team and the other a Franco-German collaboration.  The authors of both studies claimed that their “purified” material contained some particles that were HIV particles.  However they admitted that their material predominantly contained “budding membrane particles frequently called microvesicles” or “mock virus”.  In other words, the “HIV” proteins have been and still are obtained from particulate material which consists overwhelmingly of cellular fragments in which are interspersed a small number of particles whose morphology more resembles that of retrovirus particles but none of which have all the structural characteristics attributed to HIV or even to retrovirus particles.26 27


The minimum absolutely necessary but not sufficient condition to claim that what are called "HIV-1 particles" are a retrovirus and not cellular microvesicles is to show that the sucrose density fractions obtained from the infected cells, the “purified virus”, contain proteins which are not present in the same fractions obtained from non-infected cells, the “mock virus”.  However, this is not the case.  The only difference one can see in the SDS-polyacrylamide gel electrophoresis strips of "purified virus" and "mock virus" is quantitative, not qualitative.  This means that the same proteins are present in the “purified virus” and “mock virus”.  In other words, the antigens in the antibody tests could be nothing more than cellular proteins, a problem which has been known for many years.


In 1983, Montagnier and his colleagues found a protein p45 (p41) in their “purified” virus and the protein reacted with antibodies present in the patient’s sera.   They concluded that the protein was not viral but the cellular protein actin,28 a view still held by Montagnier.29  At present, some of the best known HIV experts acknowledge that the proteins with molecular weight of approximately 41,000 present in the “purified HIV” are in fact actin.30  In 1989 researchers from New York showed that p120 and p160 in the “purified virus” are oligomers of p41.31


In 1987  Henderson isolated the p30-32 and p34-36 of "HIV purified by double banding" in sucrose density gradients.  By comparing the amino-acid sequences of these proteins with Class II histocompatability DR proteins, they concluded that "the DR alpha and beta chains appeared to be identical to the p34-36 and p30-32 proteins respectively".32 That these proteins are cellular is acknowledged by other HIV experts.30


Since the antigens present in the antibody test kits are normal cellular proteins, it follows that they will react with auto-antibodies.  They may also cross-react with other antibodies including HIV which may be present in the sera.  However the only way to prove that HIV antibodies are present in any sera is by using HIV as a gold standard which to date has not been done.  Until this is achieved, the HIV prevalence in South Africa cannot be ascertained – it could be anything from zero to five million.


This does not mean there is no relationship between a positive “HIV” antibody test, whatever its genesis, and the risk of developing AIDS.  In fact there can be no doubt that in the risk groups many studies have proven this an undisputed fact.  However, at present there is no proof that the reason for being seropositive is HIV.  A positive antibody test may be no more than a non-specific marker reflecting a propensity to develop certain illnesses.  In this manner it can be regarded as having similar clinical utility to measurements of the erythrocyte sedimentation rate (ESR).  The ESR, although archetypically non-specific, is highly indicative or predictive of morbidity and mortality.  In fact the ESR is a far better predictor of AIDS than the CD4 count despite the fact the latter is accepted to be the cause of the clinical AID syndrome.21 33


We agree with Fassin and Schneider “to widen the debate and hence to increase understanding of the epidemic” in South Africa.    However, as well as debating the “social epidemiology of HIV”, the debate must be preceded by or at least be concurrent with the “biomedical and behavioural” debate.    Once it is irrefutably proven that HIV has indeed infected 5 million or any number of South Africans as a result of heterosexual transmission or by any other means, then it would be useful to pursue the “social epidemiology of HIV”.


Eleni Papadopulos-Eleopulos  Biophysicist, Department of Medical Physics, Royal Perth Hospital, Perth, Western Australia


Valendar F. Turner  Consultant Emergency Physician, Department of Emergency Medicine, Royal Perth Hospital, Perth, Western Australia


John M Papadimitriou  Professor of Pathology, University of Western Australia, Perth, Western Australia


Barry A. P. Page  Physicist, Department of Medical Physics, Royal Perth Hospital, Perth, Western Australia


Sam Mhlongo  Head & Chief Family Practitioner, Family Medicine & Primary Health Care, Medical University of South Africa, Johannesberg, South Africa


Helman Alfonso  Department of Research, Universidad Metropolitana Barranquilla, Colombia


David Causer Physicist, Department of Medical Physics, Royal Perth Hospital, Perth, Western Australia


Christian Fiala  Gynaecologist, Mollardgasse 12a A-1060 Vienna, Austria


Anthony Brink  Advocate of the High Court of South Africa





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Competing interests:   None declared