Sex, Race, HIV/AIDS and the African Problem by The Perth Group

SEX, RACE, HIV/AIDS AND THE AFRICAN PROBLEM

Eleni Papadopulos-Eleopulos1, Valendar F. Turner2, John M. Papadimitriou3, Sam Mhlongo4, Helman Alfonso5, David Causer6, Barry Page6

1Corresponding author, Biophysicist, Department of Medical Physics, Royal Perth Hospital, Wellington Street, Perth 6001, Western Australia

2Consultant Emergency Physician, Department of Emergency Medicine, Royal Perth Hospital

3Professor of Pathology, University of Western Australia

4Dr. Sam Mhlongo details

5Head, Department of Research, Universidad Metropolitana Barranquilla, Colombia

6Physicist, Department of Medical Physics, Royal Perth Hospital

SUMMARY

The data pertaining to the relationship between sexual activity and HIV infection and AIDS, especially that applicable to Africa, is critically analysed. It is concluded that: (i) no proof exist that “HIV”/AIDS is bidirectionally sexually transmitted; (ii) like pregnancy, a positive “HIV” antibody test and AIDS, can only be sexually acquired. 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. The notion that HIV/AIDS is sexually transmitted disease and is amenable to “anti-retroviral agents” is in urgent need of revision.

SEXUAL TRANSMISSION IN GAY MEN

In 1981 high frequencies of two uncommon diseases, Pneumocystis carinii pneumonia (PCP) and Kaposi’s sarcoma (KS), were reported in gay men. Because these men were extremely promiscuous the hypothesis was put forward that the underlying cause may be a sexually transmitted agent. This prompted epidemiological studies designed to study the relationship between these diseases and a range of demographic variables including sexual practices. The first results of this type of study employing healthy gay men as controls were published in 1982. The authors reported that: “The distributions of the number of different sex partners per month in different time periods before disease showed that patients were more promiscuous than controls. 50% of patients reported having sex with 10 or more different partners during an average month in the year before onset of disease, compared with 17% of controls. Some reported extreme levels of sexual activity: the most promiscuous patient estimated that he had had sexual intercourse with an average of 90 different partners per month in the year preceding disease”.1. In a more detailed study by the same authors published in 1984 it was reported that: “Stepwise logistic regression analysis indicated that the number of partners per month in receptive anal-genital intercourse with ejaculation, the number of occasions of “fisting” [“the insertion of a fist or forearm into the partner’s anus or rectum”], and cytomegalovirus antibody titers were the only independent and statistically significant variables for discriminating patients from controls”.2 In the same year Robert Gallo announced the discovery of a new retrovirus, HTLV-III (HIV) as well as antibody tests for the virus, and concluded these data “provided clearcut evidence that the aetiology of AIDS and ARC [AIDS related complex] was the new lymphotropic retrovirus, HTLV-III”.3

At the same time Gallo’s group published studies in which the relationship between a positive antibody test and sexual activity was evaluated. In one such study one reads: “Seropositivity to HTLV-III was significantly associated with travel to the United States…Increased frequency of anal receptive intercourse was also independently associated with seropositivity”.4 In another study they wrote: “Of eight different sex acts, seropositivity correlated only with receptive anal intercourse…and with manual stimulation of the subjects rectum (receptive “fisting”…)…and was inversely correlated with insertive anal intercourse” (italics ours). They concluded: “These data suggest that frequent receptive anal intercourse with many homosexual partners predisposes to HTLV-III infection with the consequent emergence of lymphadenopathy and the various manifestation of lesser and fully fledged AIDS”.5 Two years later Gallo and his colleagues 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”.6 Thus by late 1984 the available evidence suggested an extremely significant difference between all the other sexually transmitted infectious agent/diseases and a positive HIV antibody test/AIDS.

Unlike all other sexually transmitted agents/diseases which are bidirectionally transmitted, (that is, from the insertive partner (heterosexual men or insertive gay men) to the passive partner (women, passive gay men), the only sexual risk factor for the appearance of AIDS and a positive HIV antibody test is passive anal intercourse. This observation presents the following possibilities:

(a) HIV is an infectious agent unlike any other. The insertive (active) partner transmits HIV to the passive partner but, since the passive cannot transmit it to the active partner, the latter must acquire infection by other means;

(b) The antibody tests do not prove HIV infection. Both AIDS and “HIV” antibodies are related to passive anal intercourse but the factor(s) which cause them have nothing to do with a retrovirus, HIV;

(c) As Gallo et al pointed out, unless their findings are confirmed by other groups, the possibility “that the virus may be transmitted by sexual activities other than receptive rectal intercourse, although probably with lower efficiency” cannot be excluded.

The third possibility, (c), has been excluded by many studies, including from Amsterdam, The University of California and the Pasteur Institute, which confirmed Gallo et al’s findings. These researchers also found that “rectal receptivity with most or all partners versus none or one partner were statistically significant, independently of the number of partners”7 and “the number of partners is far less important than the kind of sex they practice”.8 Thus, it is not the number of different partners but the number of episodes of receptive anal intercourse, which is directly related to seroconversion.

As researchers from the University of California and the San Francisco Department of Health pointed out in 1993, although “The detection of the etiological agent human immunodeficiency virus (HIV) in 1983 and its isolation in semen in 1984 provided biological support for the theory that AIDS is a sexually transmitted disease”, not one study has “documented statistically significant independent association between HIV infection and insertive anal intercourse (IAI), receptive oral intercourse (ROI), or insertive oral intercourse (IOI)”. In their analysis of 83 seroconversions which occurred between 1984 and 1989 in three San Francisco cohorts of homosexual and bisexual men they reported: “As did many previous studies in homosexual men, we found receptive anal intercourse and elevated number of intercourse partners to be of highest risk for HIV seroconversion. We also found some evidence indicating receptive oral intercourse to be unsafe, as recent case reports have suggested…These findings should be incorporated into HIV prevention and safe sex education efforts so that individuals are aware of which sexual practices are safe and which are unsafe”.9

Undoubtedly, to date the most comprehensive and informative data from studies conducted in gay men have been obtained from the Multicenter AIDS Cohort Study (MACS), the largest (4954 gay men enrolled) which commenced in 1984 and is ongoing. In one of several papers published in 1983 the authors reported that: “Overall, the prevalence of antibodies to human immunodeficiency virus (HIV) in these men was 38.0%. The factor most strongly associated with prevalent HIV infection according to a multiple logistic regression model was rectal trauma, a composite variable which included receptive anal fisting, enemas before sex, reporting of blood around the rectum, and the observation of scarring, fissures or fistulas on rectal examination. Receptive anal intercourse also was strongly associated with HIV infection in the model…Most striking, however, was the strong association with HIV antibody positivity of enema usage, receptive fisting, and receptive anal intercourse with most or all partners. Almost 90% of 138 men in this combined category had antibodies to HIV”.10

In another paper published in the same year: “2507 homosexual men who were seronegative for human immunodeficiency virus (HIV) at enrolment were followed for six months to elucidate risk factors for seroconversion to HIV. 95 (3.8%) seroconverted. Of men who did not engage in receptive anal intercourse within six months before baseline and in the six-month follow-up period, only 0.5% (3/646) seroconverted to HIV…On multivariate analysis receptive anal intercourse was the only significant risk factor for seroconversion to HIV, the risk ratio increasing from 3-fold for one partner to 18-fold for five or more partners. Furthermore, data for the two successive six-month periods show that men who reduced or stopped the practice of receptive anal intercourse significantly lowered their risk of seroconversion to 3.2% and 1.8%, respectively. Receptive anal intercourse accounted for nearly all new HIV infections among the homosexual men enrolled in this study, and the hazards of this practice need to be emphasised in community educational projects”.

With regard to seroconversion in three men who did not admit to practising passive anal intercourse the authors wrote: “These data suggest a low (less than 1% six-month) risk of seroconversion due only to the practice of insertive anal intercourse. Alternatively, this may reflect misclassification of the men who actually did participate in receptive anal intercourse”.11 In addition to “misclassification” the positive antibody test in these three men may be due to:

a) the use of IV drugs or even non IV drugs such as nitrites which have been found to be associated with seroconversion in most, if not all, studies in gay men, including that of Gallo et al 1984; or to the use of cocaine which is also associated with seroconversion;12

b) false positive results. No antibody test is 100% specific and the criteria for a positive antibody test used by the authors of this study are not sufficient to prove infection anywhere else in the world.

In yet another report from the MACS published in 1989; “A total of 2,915 men who had no evidence of HIV-1 antibody at baseline completed at least one follow-up visit in addition to the baseline visit. Two hundred and thirty-two (8%) of these seronegative men became antibody positive to HIV-1 within the subsequent 24 months. The proportion of men who seroconverted differed greatly according to the specific sexual activities in which they reported engaging during the 12 months prior to the first antibody positive visit…This study reconfirms the very strong association between receptive anal-genital intercourse and risk of infection by HIV-1. The study also raises the possibility that there is a low risk of infection to the insertive partner in anal-genital intercourse [Ten of the 232 men who seroconverted denied passive intercourse] …suggest that infection may rarely occur through sexual activity other than anal-genital intercourse” (two men who seroconverted denied anal-genital intercourse). In regard to the ten men who became positive they wrote “one cannot completely exclude the possibility that these men either preferred not to or forgot to report receptive activity”. Regarding the two men who denied anal-genital intercourse, they authors wrote, “Many of the men not engaging in anal-genital intercourse, however, were still sexually active, often with exposure to semen” and that “The accuracy of this report, of course, is dependent upon the accuracy of recall of the individual. The motivation for denial of anal-genital intercourse increases as it becomes more and more apparent to the homosexual community that this is the major route of infection”. If this is the case for anal intercourse in general, it should be even more for the practice of passive anal intercourse. In addition, the criteria used to define a positive antibody test in this study are also not sufficient to diagnose HIV infection anywhere else in the world.13

In yet another report from the MACS published in 1992, seropositive gay men were divided into two groups: Group A, who developed AIDS and group B, who did not develop AIDS five years post seroconversion. Unlike other sexually transmitted diseases, the authors found that: “receptive anal intercourse both before and after seroconversion with different partners was reported more frequently by men with AIDS…When group A was stratified by development of AIDS within 30 months and within 30-60 months and compared to matched controls, a greater proportion of high-risk sexual activities postseroconversion was noted in the group progressing to AIDS most rapidly. The differences were statistically significant 12 and 24 months post seroconversion”. It was concluded: “These data then suggest that greater sexual activity following establishment of HIV-1 infection leads to exposure to promoters or co-factors that augment (or determine) the rate of progression to AIDS”14 (italics ours).

In 1994 Carlos Caceres and Godfried van Griensven published a review of all the studies in gay men which examined the relationship between sexual activities and the development of immune deficiency, KS, PCP, and AIDS conducted before the discovery of HIV and, since its discovery, nearly all the studies including the MACS, between sexual activities and “HIV infection”. They concluded that the studies conducted prior to HIV, “identified anogenital receptive intercourse and the number of sexual partners as risk factors for immunodeficiency, for the presence of KS, Pneumocystis carinii pneumonia (PCP) and AIDS”. Summarising the evidence on the relationship between sexual activities and HIV seroconversion they wrote: “It can be said that the cited reports yield convincing evidence that (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, biologic plausibility, credible case reports and some studies show a modest risk, detectable only by with powerful designs; (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”.15

Since heterosexual men are only insertive, the above data demonstrate that HIV cannot be heterosexually transmitted. The only alternative explanation is an ability for HIV to discriminate between gay and heterosexual men.

HETEROSEXUAL TRANSMISSION

Male to female transmission

The first study which claimed to “clearly demonstrate that receptive anal intercourse was not a requirement” for HIV/AIDS transmission and to provide “evidence for both male-to-female and female-to-male transmission of infection and disease” was published by Gallo and his associates from the Walter Reed Army Medical Center, including Robert Redfield, in 1985. Of 41 patients with AIDS or AIDS related complex who had a positive antibody test, in 15 cases (37%) “HTLV-III infection appeared to have been heterosexually acquired”. Five of the patients were women (3 black, 2 hispanic, and 10 were men (1 hispanic, 2 whites and 7 blacks)).16 Also in 1985 Gallo and his colleagues published another paper, this time with data from Rwanda, in which they also claimed proof for heterosexual transmission. They tested 33 prostitutes, 25 consecutive male customers of prostitutes, as well as 27 male and 33 female controls. Twenty nine (88%) of the prostitutes, 7 (28%) of the males customers as well as 4 (12%) and 2 (7%) of the female and male controls respectively were found positive.17 The collection and interpretation of the data in these studies were severely criticised by many, including Nancy Padian who attempted more than anyone else to prove heterosexual transmission of HIV.18-25

Suffice to quote one criticism. Discussing the study from the Walter Reed Center, the editors of the book ‘AIDS and Sex’ published in 1990, wrote “In another case, government researchers published data indicating that United States armed forces personnel infected with HIV-1 had caught the virus from prostitutes, triggering calls for increasing campaigns against prostitution. When infected soldiers were interviewed by nonmilitary researchers, whom they trusted, it became clear than nearly all had been infected through intravenous drug use or homosexual contact, acts for which they could be expelled from the armed services, which prevent them from being candid with the original military researchers. In each of these flawed published studies, researchers, journal editor, and peer reviewers failed to correct mistakes that should have been recognized”.26

Nonetheless, Gallo and his colleagues insisted that they had provided “scientifically sound evidence for bidirectional heterosexual transmission…Human T-cell lymphotropic virus type III is bidirectionally sexually transmitted disease”.27 However, data from the largest epidemiological studies published since then do not support this claim despite the fact that most are cross-sectional. The largest European study, the heterosexual multicentre study (nine centres from six countries), was in two parts, cross-sectional and longitudinal. In the first publication, from the cross-sectional part in 1989, the authors reported that: “The rate of male-to-female transmission was 27%…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”.28 In the 1992 update of the European Study Group on Heterosexual Transmission of HIV, 20% of the female partners of HIV positive men were found positive and the same risk factor, anal intercourse, was again confirmed.29 Similar findings were reported in a study from New York City: “Our study demonstrates that health of the index, anal intercourse and bleeding as a result of intercourse are the major determinants of sexual transmission of HIV to women”.30

In two studies, one from the UK and the other from Italy, anal sex was associated with an increase in seroconversion, but the difference was not significant.31, 32 However, in one of the studies consisting of a total of 343 women, 19 of whom seroconverted, three occurred in couples who always used condoms.32 In the other study “seropositive and seronegative [women] did not differ in terms of frequency of protected or unprotected vaginal intercourse” or “number of acts of vaginal intercourse” with their seropositive partner. These findings are at odds with all which is known about other sexually transmitted agents, and suggest that the cause of the seroconversion may have been other than sexual intercourse.

The claim that HIV is a heterosexually transmitted virus is also markedly inconsistent with the data obtained from studies of female prostitutes. Even if, as it is widely accepted, by some unknown means a sexually transmitted infectious agent found its way into the promiscuous portion of the gay male population in certain large cities in the United States in the late 1970s, given the facts that prostitutes are frequented by bisexual men and, at the very earliest, “safe” sexual practices date from 1985, one would have expected HIV/AIDS to have spread rapidly through prostitutes and thence to the general community. However, the prevalence of “HIV” antibodies amongst prostitutes is almost entirely confined to those who admit to being drug users. Virtually all others remain free from “HIV” antibodies.

In September 1985, 56 non-intravenous drug using (IVDU) prostitutes were tested “In the rue Saint-Denis, the most notorious street in Paris for prostitution. More than a thousand prostitutes work in this area….These women, aged 18-60, have sexual intercourse 15-25 times daily and do not routinely use protection”. None were positive.33

In Copenhagen, 101 non-IVDU prostitutes, a quarter of whom “suspected that up to one fifth of their clients were homosexual or bisexual”, were tested during August/October 1985. The median numbers of sexual encounters per week was 20. None were positive.34

In 1985, 132 prostitutes (and 55 non-prostitutes) who attended a Sydney STD clinic were tested for HIV antibodies. The average numbers of sexual partners (clients and lovers) in the previous month was 24.5. When an estimate was made to separate clients and lovers, the median number of sexual contacts per year rose from 175 to 450. The partners of only 14 (11%) of prostitutes used condoms at all and 49% of their partners used condoms in fewer than 20% of encounters. No women were positive.35

The same Australian Clinic repeatedly tested an additional 491 prostitutes who attended between 1986 and 1988. Of 231 out of the 491 prostitutes surveyed, 19% “had bisexual non-paying partners and 21% had partners who injected drugs. Sixty-nine percent always used condoms for vaginal intercourse with paying clients, but they were rarely used with non-paying partners. Condoms were rarely used by those clients and/or partners for the 18% of prostitutes practising anal intercourse”. No women were positive.36 At the time of this report, a decade into the AIDS era, the authors commented, “there has been no documented case of a female prostitute in Australia becoming infected with HIV through sexual intercourse” (italics ours). Yet, these investigators from the Sydney Sexual Health Centre concluded “there are still many women working as prostitutes in Sydney who remain seriously at risk of HIV infection”.

In Spain, of 519 non-IVDU prostitutes tested between May 1989 and December 1990, only 12 (2.3%) had positive test, which was “only slightly higher than that reported 5 years ago in similar surveys”. Some prostitutes had as many as 600 partners a month and the development of a positive antibody test was directly related to the practice of anal intercourse. The authors also noted, “a more striking and disappointing finding was the low proportion of prostitutes who used condoms at all times, despite the several mass-media AIDS prevention campaigns that have been carried out in Spain”.37

Data from two Scottish studies,38 the 1993 “European working group on HIV infection in female prostitutes study”39 and a 1994 report of 53,903 Filipino prostitutes tested between 1985 to 1992, confirm that non-IVDU prostitutes remain virtually devoid of HIV infection. For example, in the latter study, only 72 (0.01%) women were found to be HIV positive.40

In studies where there appear to be a high incidence of HIV amongst prostitutes there are uncertainties that defy explanation. For example, although “HIV has been present in the commercial sex work networks in the Philippines and Indonesia for almost as long as it has been in Thailand and Cambodia”, the prevalence of HIV in the former is 0.13% and 0.02% respectively and 18.8% and 40% in the latter.41 If these data are accurate the discrepancy defies epidemiological explanation and had indeed baffled the experts although the latter postulate “behavioural factors” such as one country’s prostitutes and clients being considerably more or less sexually active than another. Be that as it may, since 5674 (44%) and 4360 (34%) of the 12785 Cambodian “HIV and AIDS Case Reports” till 31/12/97 are listed as “Unknown” gender and age, data collection at least by the WHO in Cambodia, must be regarded problematic.42

Transmission to female partners of haemophiliacs

It is a fact that “most of the persons who have acquired AIDS through heterosexual contact are the female sexual partners of intravenous (IV) drug users”, some of which “may belong to high-risk groups through their own lifestyles, for example, prostitution and IV drug use”, but do not admit such practices. Because of these and because from the very beginning the highest rate of positive antibody tests was found in haemophiliacs and “the female sexual partners of haemophiliacs, in general, are healthy and have no other known AIDS risk factors”,43 from the time when HIV antibody tests were introduced, many studies were conducted in which the sexual partners of haemophiliacs were tested. The reported rates in these women varied from 0-19%.{Kreiss, 1985 #1323; Allain, 1986 #808; Biberfeld, 1986 #1351; Jason, 1986 #373; Anonymous, 1987 #1371; 44-50

However, most of these studies were published before 1990, using criteria which today are not considered sufficient to prove HIV infection; these studies are cross-sectional and small or merely case reports. The latter included a report by Luc Montagnier and Francoise Barre-Sinoussi, the discoverers of HIV, and their associates. The wife of an HIV positive haemophiliac who practised vaginal, oral and anal intercourse was found to be seropositive and to have immune deficiency (low T4 lymphocytes). 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 despite “once infected with HIV, always infected”.51

The first study in haemophiliac partners was conducted by researchers from Denmark and the USA. Of nine female spouses or regular female sexual partners (mean duration of conjugal relationship 14.2 years), one was found positive and practised vaginal, oral and anal intercourse. The authors concluded: “This study shows that heterosexual transmission of HTLV-III as detected by positive tests for HTLV-III antibody can occur between haemophiliacs and their sexual partners. Furthermore, it suggests that HTLV-III infection may be facilitated by the practice of anal intercourse, as it appears to be in homosexual men”.52

The largest study of haemophiliac female sexual partners was published by a researcher from the USA. Between August 1985 and February 1989, “the Transfusion Safety Study has enrolled persons with all forms of congenital clotting disorders into a long-term follow-up at Clinical centres in New York, Miami, Detroit, Seattle, San Francisco and Los Angeles”, as well as 201 female sexual partners. At entry into the study 21 of the females were positive. “Of the 180 enrolled sexual partners anti-HIV-1 negative at entry, 151 (84%) were seen in follow-up over an interval ranging from 5 to 47 months. The total period of longitudinal observation for these 151 contacts was 351 person-years, a mean of 2.3 years per person. None seroconverted. During follow-up, 13 (8%) of the 151 women became pregnant”. Detailed questionnaires concerning sexual practices were completed by 50 (28%) of the 180 seronegative women. “Of the 47 who reported vaginal intercourse, 6 (13%) stated they always used a condom. Twenty (42%) said that their partner sometimes or usually used a condom, and 21 (45%) said they never used a condom in vaginal intercourse”. In the 1991 publication where the authors discuss their findings as well as those of others they wrote: “All of the infections observed in partners of haemophiliacs in this study and all but two of the other studies cited, occurred prior to first observation [cross-sectional studies]. Only five seroconversions have been documented prospectively, with the most recent of those having occurred in 1986.

Commenting on the discrepancy between the findings in the cross-sectional studies and the prospective studies they wrote: “These two circumstances may be explained by awareness of risk earlier in the course of infection and more extensive modification of their sexual practices than among other heterosexual risk groups. The large majority of haemophiliacs treated with factor VIII concentrates in this and other studies become infected essentially as a cohort between 1981 and 1983, a period during which sexual practices would not have been modified. By late 1983 to early 1984, however, haemophilia clinics were aware of risk of infection associated with concentrates and the potential for transmission to sexual partners. Counselling was provided to this group much earlier than other heterosexual risk groups. On the other hand, the information from our questionnaire indicates that sexual practices capable of transmitting HIV-1 have persisted among haemophiliacs and their partners. Although we had responses from only a minority (28%) of the seronegative women, it seems likely that any bias in willingness to provide information would be toward participation by those most likely to have conformed to approved behaviour. In addition, unprotected sexual contact during the period of follow-up was evidenced by the occurrence of 13 pregnancies among women who remained seronegative. Without questioning that sexual practices have been made safer by counselling there has been enough opportunity for sexual transmission to make counselling seem an inadequate explanation for the virtual absence of prospectively observed seroconversions”.53 In fact no seroconversions occurred in the best designed and executed studies.

Researchers from the Netherlands conducted “a three year follow up study of 13 haemophiliacs positive for HIV antibody and their spouses”. The “patients had had different stages of HIV, including AIDS, for three to five years”. All couples practised vaginal intercourse, two during menstruation, 4 partners had oral intercourse. One man had used condoms before becoming positive and 4 started to use condoms after being told that the man was positive. No women became positive. They “calculated that in 11 couples unprotected vaginal intercourse occurred a maximum of 2,250 times (minimum 1,563) without transmission of HIV; for protected vaginal intercourse the figures were 1,252 and 942 respectively”.54

In another study, “Follow-up testing was performed on 18 of the sexual partners to determine whether they had seroconverted with longer heterosexual exposure. Eight partners have been tested twice, five have been tested three times, and two have been tested four times. All follow-up samples have remained seronegative after ELISA and Western blot test…Before 1984, six couples used condoms and only two of these used them regularly. Although during 1987 the number of couples using condoms has increased through risk-reduction education, it does not seem that the lack of seropositivity in the spouses is due to a disproportionately higher use of barrier contraceptive devices. While the exact number of sexual encounters is unknown, only three of 36 sexual partners reported curtailing their sexual activities due to fear of AIDS”. 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”.55

Female to male transmission

The most common route of transmission of the sexually transmitted agents is via prostitutes. Indeed, this was the route by which Gallo et al claimed all the men documented in their 1985 papers were infected. However, in 1989 two well known HIV experts wrote; “no case has been confirmed of direct transmission from a female prostitute to a male partner”.56 This, despite the fact that a significant proportion of prostitutes are infected as a result of intravenous drug use, and were so even before education concerning safe sex practices was introduced.

The reported studies for female to male transmission, unlike those for male to female transmission, are limited. In 1985 four women were reported from Australia to have become infected as a result of artificial insemination. “All four husbands have remained antibody negative, despite regular sexual contact without the use of condoms for up to three years”57 In 1988 researchers from the Centre for Disease Control and the New York Health Department in a cross-sectional study reported that 2 out of 25 husbands of women “with Transfusion-Associated Infection became infected”.58 Between February 1, 1987 and December 31, 1992 researchers from Milan, Italy and Colombia University, New York, recruited infected women from eight hospital departments of infectious diseases, five IV drug clinics and three HIV Surveillance Centres. Each of the partners who was not already known to be infected was tested. “Of the 275 men interviewed and tested for HIV antibodies, 22 were excluded from the study because these men reported promiscuous behaviour or homosexual contacts. The prevalence of HIV infection was 31.8% in this group (seven cases). Of the remaining 253 couples 11 were excluded because no risk was evident in the women, thus making it impossible to assign the direction of transmission. The prevalence of HIV infection was 18.2% in this group (two cases). Of the 242 couples remaining, 18 reported not to have had sexual intercourse during at least 1 year and were also excluded from the study. The prevalence of HIV infection was 33.3% in this group (six cases)”. Of the remaining 224, 14 tested positive. “Peno-anal intercourse was the strongest behavioural risk factor.” Discussing these findings the others wrote; “A possible explanation for our present findings is some misclassification of male-to-female as female-to-male transmission, which may have occurred because of the cross-sectional nature of the study design”.59

The results of the longitudinal study of female to male transmission of the Multicenter European Study Group on Heterosexual Transmission of HIV which started in March 1987, were reported in 1994. Of the 378 couples, 256 continued to have sexual relationships after recruitment. “The 256 couples were classified according to the frequency of condom use during follow-up. Only 124 couples (48.4 percent) used condoms for every episode of vaginal or anal intercourse (consistent condom users); 121 couples (47.3 percent) did not always use condoms (inconsistent condom users). Among the 121 couples who were inconsistent users, 61 (50.4 percent)) used condoms for at least half their sexual contacts but not for every contact, and 60 (49.6 percent) rarely or never used condoms. Eleven of the 256 couples (4.3 percent) refused to answer questions about their sexual behaviour, although the uninfected partners agreed to follow-up serologic testing.” Four partners of 93 infected women seroconverted.60 “No seroconversion occurred among the 124 couples who used condoms for each vaginal or anal contact”.60

In 1990, Al-Nozha et al tested the husbands of four women, two with AIDS related complex and the other two with AIDS all of whom became infected following blood transfusion. All remained healthy and negative “even after 4-5 years of sexual exposure”.61

Nancy Padian et al study on heterosexual transmission

In the United States, and in fact anywhere in the world, the most thorough investigation of heterosexual transmission was carried out by Nancy Padian from the Department of Epidemiology and Biostatistics, University of California, and her associates. Their ongoing study started in 1985. In 1987 they reported their study of men to women transmission. At entry into the study of 97 women, 22 (23%) were found positive. The rate of positivity was higher (42%) in women who were partners of IV users. “Approximately 40% of the 75 seronegative women were re-tested six months after entry into the study; some had seroconverted”. “Regardless of risk groups of index case”, (bisexual, haemophiliac, “men infected from contaminated transfusions”), “seropositive women were 4.6 times more likely than seronegative women to have had more than 100 sexual exposures with their infected partner”. “Anal intercourse significantly discriminated between seronegative and seropositive women”. Because three of the women who tested positive admitted to neither IV drug use, oral or anal intercourse, the authors concluded that HIV can be transmitted via vaginal intercourse.62 At the Fourth International Conference on AIDS, 1988, Padian and her colleagues reported that; at entry: “Infection rate was 24% (95% confidence interval=18%-32%). In multivariate analysis, only the practice of anal intercourse (p=.003) and non-white race (p=.015) were significantly associated with infection…We have also enrolled male partners of infected women. In spite of repeated unprotected sexual intercourse (median number of sexual contacts=399) none of the twenty male partners was infected”.63

Because “AIDS epidemiologists may not have the opportunity to collect data on a regular basis and are thus forced to rely on retrospective reports of behaviour even though the accuracy of these reports (especially for a variety of sexual practices) has not been established”, Padian tried to establish a correlation between the answers given by the men and women regarding sexual practices. “The total number of vaginal intercourse contacts reported by the men and the women were highly correlated (rr=0.84…). Number of anal intercourse contacts was compared as a continuous variable, with somewhat less strong agreement (r=0.44…)” [In fact this is a poor agreement] “. In addition, according to Padian, “measurements were not independent because couples may have discussed responses prior to the interview”, the “couples knew they were to be interviewed about their sexual behaviour”.64

In 1991, six years after the study commenced, Padian and her colleagues reported their data on female to male transmission. Of 72 males “non-drug-using” partners of infected women, recruited in the above period, they “observed one probable instance” of female-to-male transmission. They gave a number of reasons for considering this case as indefinite (“probable”). To this one must add the fact that the criteria they used (“antibodies to p24 (core polypeptide) and or gp41”) are at present not considered sufficient to prove HIV infection in most countries, institutions or laboratories. Discussing the discrepancy between their findings and those of other investigators, including those of Redfield and Gallo, they stated that the other “studies may not have adequately controlled for other confounding nonsexual routes of transmission such as risks associated with intravenous drug use. At first blush, cases that appear attributed to heterosexual transmission may, after in-depth interviewing, actually be linked to other sources of risk…because partner studies are by definition not random samples, and most reported results are based on retrospective or cross-sectional analyses, some studies may overselect couples in which both partners in a couple are infected because such couples may be more easily identified, thus biasing transmission rates. Furthermore, it is often difficult to establish the source of infection in such couples”.65

In 1997 Padian published a paper entitled “Heterosexual Transmission of Human Immunodeficency Virus (HIV) in Northern California: Results from a Ten-Year Study”. The data was divided in two parts, cross-sectional and prospective and every effort was made to exclude confounding variables such as drug use. In the cross-sectional study they reported an overall 19% male to female transmission from which they estimated that: “infectivity for male-to-female transmission is low, approximately 0.0009 per contact” (1/1111) and “approximately eight-times more efficient than female-to-male transmission”. They also reported a 2.4% (two men out of 82) rate of female-to-male transmission. Of these two men one was, the “probable” transmission reported in 1991 and doubts were also expressed about the second man. Using their estimate of approximately 1/9000 for female-to male transmission, it would take 6000 sexual contacts to reach a probability of 0.48 of becoming infected. If we hypothesise that sexual activity commences at age 20 and takes place on average three times weekly thereafter, the man would be approaching his sixties by the time he attained this risk. Discussing their findings they wrote: “To our knowledge, our study is the largest and longest study of the heterosexual transmission of HIV in the United States. The consistency of results over the 10-year duration argues for the validity of our results. For example, the practice of anal sex and lack of condom use have remained strong predictors of transmission since the beginning of the study…Higher rates of heterosexual transmission, particularly from females to males, reported in other studies may be due to a number of factors… Misclassification of mode of transmission may be an especially important factor to consider, particularly when interpreting estimates of the rate of female-to-male sexual transmission, because women who are injection drug users themselves are more likely to have a male injection drug user partner than vice versa. Studies in Europe and the United States which have reported higher rates of female-to-male transmission include relatively higher rates of female injection drug users and their sex partners.”

In the prospective study of 175 HIV-discordant couples, tested every six months, not one of the 175 non-infected men or women became HIV positive. Discussing their findings they stated that the absence of infection “over the course of the study cannot be entirely attributed to significant behaviour change.” Indeed, although the couples received extensive and continuous safe sex education, and although “At last follow-up were much more likely to be abstinent or to use condoms constantly, and were much less likely to practice anal intercourse”, even then 25% of the couples were not using condoms “consistently”.66

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) The frequency of this practice, by either sex, and not the number of partners (promiscuity) is the risk factor for the development of AIDS and of a positive antibody test.

c) 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”26 which is of critical importance. Thus AIDS and a positive antibody test, like pregnancy, 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. AIDS is more like anal67, 68 and cervical cancer.69 The effect is not the result of the act itself but its high frequency. But, as with pregnancy and cervical and anal cancer, other factors may promote or militate against the development of AIDS.

AFRICAN DATA

In his book “Viral Sex”, Jaap Goudsmit, one of the most eminent HIV/AIDS experts, declared that for heterosexual HIV transmission “a homosexual or anal factor seems to be required. In Haiti, for example, HIV was probably introduced by gay tourists from the United States who sought sex with young male prostitutes. The Haitian men they infected with HIV-1B then infected wives and girlfriends, particularly since heterosexual couples in Latin America commonly use anal sex as a ‘no cost’ contraceptive measure…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….”.8

If in Africa, as everywhere else, receptive anal intercourse is the risk factor for acquiring AIDS and a positive antibody test, then in Africa, as everywhere else, there should be no heterosexual epidemic of HIV/AIDS. Yet it is claimed that tens of millions of heterosexual Africans have HIV/AIDS and that there is a 1:1 sex ratio.

There are three possibilities to account for this discrepancy:

(a) Goudsmit is wrong and in Africa unlike anywhere else, HIV is:

(i) transmitted by vaginal intercourse;

(ii) bidirectionally transmitted from male to female and from female to male.

In other words HIV discriminates between races and/or continents. South Africa would be the ideal example of this highly specific racial behaviour of HIV.

(b) A much higher proportion of African men are bisexual and practise much more passive anal intercourse than bisexuals in other parts of the world. In other words a very high proportion of African men must be as sexually active as the small minority of non-African gay men who have positive antibody tests and develop AIDS.

© The data and the interpretation of a positive antibody test and/or AIDS, or the definition of heterosexual transmission in Africa is invalid.

To date no proof exists that any of the known sexually transmitted agents discriminates between races and/or continents, nor has anybody presented any actual or potential reasons to suggest HIV is an exemption. As far as the sexual behaviour of Africans is concerned, it is difficult if not impossible not to strongly infer that most of the information (scientific articles, the popular press, TV and radio on HIV/AIDS correlates strongly with the way non-Africans (particularly Caucasians) view Africans on the subject of sexual behaviour. The history of slavery and the early pre-colonial Christian missionaries created and aided and abetted the African sexual orgy stereotype which continues to pervade 21st century societies unchallenged. Most medical doctors who are in their late forties/early fifties in Europe will recall that they were taught that condoms were the answer to Africa’s poverty and such teaching was in vogue long before the advent of AIDS. There is no proof that the sexual behaviour of Africans differs from that of individuals in any other continent or race. The foremost evidence that the sexual behaviour of Africans is the same as individuals from any other race and continent is the fact that “HIV”/AIDS in Africans (and its nearly equal sex ratio) can be explained without the need to invoke promiscuity, anal intercourse or even sexual contact.

There is ample evidence that the interpretation of a positive antibody test and AIDS, as well as the definition of heterosexual transmission in Africa are invalid. According to the Centres for Disease Control (CDC), USA AIDS patients are classified as heterosexually acquiring HIV/AIDS (HT), “if they: report heterosexual contact with a person with HIV infection or at increased risk for HIV infection (US-born) or were born in countries where HT is a major route of transmission (non-US-born)”70 Thus unlike for any other sexually transmitted agent/disease for which sexual contact tracing is absolutely necessary, individuals can be said to have acquired HIV/AIDS heterosexually even if there is no proof of contact with an infected person. An African can be classified as heterosexually acquired HIV even if there is no proof that he/she has ever had sexual intercourse.70.

PROOF FOR HIV INFECTION – THE HIV ANTIBODIES

Before one introduces an antibody test into clinical practice it must be standardised and its specificity determined. There are two HIV antibody tests in common use, the ELISA (Enzyme Linked Immunosorbent Assay) and Western blot (WB). In the ELISA unseparated “HIV” proteins are attached to a solid base such as the walls of plastic tubes or microplates. The serum being tested is incubated in these containers where antibody is fixed to the solid phase antigens. After washing, enzyme labelled anti human immunoglobulin is added and also incubated. The containers are again washed and a substrate specific for the enzyme is introduced. The resulting colour change is proportional to the amount of antibody present and is read by eye, or with a spectrophotometer. For the Western blot proteins are electrophoretically separated according to molecular weight and charge. The separated proteins are then transferred on to nitrocellulose strips by a process known as electroblotting. When sera are added and the strips developed, coloured bands appear representing sites of protein/antibody reactions. Each band is designated by a small “p” for the protein followed by its molecular weight in thousands.

The WB is not standardised

Between 1983 and 1987 the detection of antibodies in patient sera which reacted with p24 or p41 (Montagnier considered p24 and Gallo p41 HIV specific) was considered proof that the patient was infected with HIV. At the same time it became obvious that a significant number of individuals at no risk of AIDS had antibodies which reacted with these proteins. For example following transfusion of negative blood 30% of patients developed at least one band, p2471 and in Australia, “20-25% of anti-HIV negative [healthy] blood donors exhibit one or more bands on a WB”.72 Because of this, since 1987 most laboratories require the presence of antibodies which react with more than one protein before the patient is considered HIV seropositive and infected with HIV. These bands include p120 and p160. Before 1987 the p120 and p160 bands could not be visualised in WB strips. This was not unexpected since p160 is accepted to be present only in infected cells, not in virus particles, and p120 to be present only in the particles’ knobs (spikes), which are rapidly lost when the particles are released from “infected” cells. Since the proteins in the WB strips are obtained from ‘purified HIV’ particles yet such particles do not possess knobs73 (p120), then neither p120 nor p160 should be present. Nevertheless in 1987, by modifying “blot preparation”, proteins of molecular weights of 120,000 and 160,000 were found which reacted with patient sera.74 However, no amount of “blot preparation” modification can create what is not already present. The explanation for the presence of these bands was elucidated in 1989 by researchers from New York who showed that in the Western blot strip, “the components visualised in the 120-160 kDa region do not correspond to gp120 or its precursor but rather represent oligomers of gp41”.75 It was also shown that the WB pattern obtained is dependent on many factors including temperature and the concentration of sodium dodecyl sulphate used to disrupt the “pure virus”. “Confusion over the identification of these bands has resulted in incorrect conclusions in experimental studies. Similarly, some clinical specimens may have been identified erroneously as seropositive, on the assumption that these bands reflected specific reactivity against two distinct viral components and fulfilled a criterion for true or probable positivity. The correct identification of these bands will affect the standards to be established for Western blot positivity: it may necessitate the reinterpretation of published results”.76 Little if any notice was taken of these findings and recommendations.

Although since 1987 most if not all countries/institutions/laboratories require the presence of more than one band on the WB to prove HIV infection, the requisite bands vary from between countries, institutions and laboratories and even between laboratories in the same country. Thus it is possible for one and the same patient to be HIV seropositive in New York but not in France or Australia. (See Table). Furthermore, as can be seen from the Table, the criteria for a positive WB in Africa are entirely different from the others. In Africa two of p160, p120, p41 are sufficient to prove HIV infection. However since 1983 Montagnier has claimed that p41 (which he calls p43 or p45) is not an HIV protein but the ubiquitous cellular protein actin.77, 78 This has been confirmed by other HIV experts such as Bess and his colleagues at the US National Cancer Institutes.79 Montagnier and his colleagues have also shown that HIV positive individuals and those at risk have high levels of actin antibodies.80 Since gp120 and gp160 are oligomers of gp41, it means that in Africa, unlike anywhere else in the world, the presence of antibodies which react with actin, a protein found in all of us, is considered proof for HIV infection.

The specificity of the antibody test has not been proven

Because all antibodies, including monoclonal antibodies cross-react,81, 82 an independent method of establishing the presence of an infectious agent for which the antibody test is to be employed must be used to prove the specificity of the test. This method is known as the gold standard83 and for the HIV antibody tests the only scientifically valid gold standard is HIV itself, that is, HIV isolation (purification). Nothing else, including the presence of absence of the clinical syndrome can be used in its place. To date there are no reports comparing the antibody tests to this gold standard and thus it is impossible to determine whether the specificity of the HIV antibody tests is zero, one hundred percent or a number in between. Yet the prevailing view is that proof of the specificity of the HIV antibody tests is firmly established. In 1985 Gallo and his associates, using the clinical syndrome as a gold standard claimed to have proven that the ELISA has a specificity of 92.6%.84 At present the specificity of the WB is considered to be virtually 100% (since the WB is not standardised it is impossible to prove its specificity even if HIV isolation were to be used as a gold standard), and for this reason ELISA is used as a screening test and the WB as a “confirmatory” test. In fact ELISA is not even reproducible. For example in a large study of healthy military applicants (1.2 million), of 12,000 positive ELISAs only 6,000 were found positive when retested. Of the later only 2,000 were WB positive.85 In other words there were 4,000 individuals who had two positive ELISAs, but a subsequent negative WB. Yet, unlike elsewhere (except England), in Africa two positive ELISAs are considered 100% specific for HIV infection.86, 87

Gallo, Montagnier and their associates were the first to perform antibody tests in Africa. In 1984 Montagnier and 19 associates tested the sera of 37 individuals from Kinshasa said to have had AIDS based on clinical grounds. “The sera were tested by ELISA and then by a RIPA (radioimmunoprecipitation assay), similar to the Western blot. The later was considered positive if a p24 band was present. The p41 band and also an 84-kDa band were not considered diagnostic because “The 43-kDa [p41] band and the 84-kDa band are cellular contaminants.” Thirty-two patients (88%) were positive, as were 6 out of 26 (23%) controls.88 Gallo et al tested 53 patients. “46 (87%) tested positive…67 (80%) of 84 prostitutes [without any clinical symptoms] and five (12.5%) of 40 and eight (15.5%) of 51 healthy controls and blood donors, respectively,” also tested positive…Sera which had one positive ELISA were considered as proof for HIV infection. Sera which had a borderline ELISA were further tested with the WB. On this test, “serum samples possessing reactivity to HTLV-III (HIV p41) and/or p24” were scored positive.89 Montagnier, Gallo as well as other experts of AIDS in Africa, who obtained similar results using a single ELISA,90 considered their positive test 100% specific for HIV infection.

In 1985 Gallo and his colleagues reported testing a number of sera collected in 1972/73 from the West Nile district of Uganda.91 These were obtained from healthy children randomly selected as controls for a study of Burkitt’s lymphoma. Both ELISA and WB were performed . Fifty of the 75 children (67%) were found to be positive. According to HIV experts these positive results are explicable by virtue of mothers infecting their children. Thus Gallo and his colleagues expected to find at least an equal percentage of adults infected. Since:

i) “Very few HIV-infected children are surviving into adulthood in good health”;92

ii) neither the children nor the adults had treatment for HIV or AIDS;

ii) the time between infection and the development of AIDS in Africa is claimed to be four years and HIV predominantly heterosexually transmitted;

then, if the tests are specific and if HIV causes AIDS, by now, few, if any Ugandans should be left alive.

In the same year, 1985 the first reports critical of HIV antibody testing in Africa began to appear. Biggar and his colleagues found that in healthy Africans the probability of finding a positive HIV antibody test increased significantly with increasing immune-complex levels. They concluded “reactivity in both ELISA and Western blot analysis may be non-specific in Africans…Serological studies from Africans would need to be re-evaluated with a more specific test before conclusions can be drawn”.93 Also in 1985 one of the best known HIV experts, Robin Weiss and his colleagues, accepted that African sera “may give a false-positive result on direct binding assay systems, or on Western blots”.94 One year later some of the best known experts on HIV/AIDS in Africa expressed the view that in Africa “…serodiagnosis is complicated by the need for confirmatory tests because of the presence of possible cross-reacting antibodies”.95

According to the World Health Organisation, “The global malaria situation is serious and becoming worse…with the incidence of malaria in the world at 300-500 million clinical cases annually. Some 1.5-2.7 million people die of malaria each year, and approximately one million deaths among children under five years of age are attributed to malaria alone or in combination with other diseases. Countries in tropical Africa account for more than 90% of the total malaria incidence and the great majority of malaria deaths”.96

As far back as 1985, Biggar and his colleagues found that in Africa a positive HIV antibody test “correlated strongly with level of antibodies against Plasmodium falciparum”, the microorganism which causes malaria.(Biggar 1985 #67) One year later, researchers from the USA and Venezuela reported that 3 out of 12 patients (25%) with Plasmodium vivax at no risk of AIDS and 5 of 12 (41%) of patients with Plasmodium falciparum, also at no risk of AIDS, ‘were found to be positive for HTLV-III/LAV [HIV] antibodies by the indirect immunofluorescence, Western blot and radioimmunoprecipitation tests, in parallel…The frequency of antibodies of HTLV-III/LAV among healthy blood donors in this area was less than 1 percent”.97

The most revealing study regarding the HIV antibody tests in Africa was published in 1994 by one of the best known retrovirologists Myron Essex, from Harvard University, and his associates. They reported that: “…leprosy patients and their contacts show an unexpectedly high rate of false positive reactivity of HIV-1 proteins on WB and ELISA”. They went one step further and proved that the antibodies which reacted with the proteins in the ELISA and WB kits were directed against two major carbohydrate-containing Mycobacterium leprae antigens-phenolic glycolipid I and especially lipoarabinomannan which is also present in Mycobacterium tuberculosis and other mycobacteria. They also suggested that at least some of the antibodies in patient sera which reacted with the proteins in the ELISA and WB may be autoantibodies.

As can be seen in their Figure 1, with the exception of one strip, all the other WB patterns obtained satisfy any criteria for a positive HIV test, including the most stringent, those in Australia. However, for Essex et al the “WB was considered diagnostic for HIV-1 if there was reactivity with two of three envelope bands (gp160/120 and gp41)”. Because of this, they claimed only strips one and two satisfied their criteria, and thus these two leprosy patients were infected with HIV while the other patients and their contacts had indeterminate WBs. However, as their figure reveals, even their “positive control” did not have a gp160 band. More importantly, and as already mentioned, gp160 and gp120 are oligomers of gp41 and their absence does not indicate a lack of reacting antibodies but rather reflects the mode of strip preparation. Even if all their WB strips displayed the gp160/120 bands, since these bands represent oligomers of actin, the presence of such bands, rather than suggesting HIV infection, would support their contention that patients with mycobacterial infections possess autoantibodies. They reported that “…WB were indeterminate in 46 (83.6%) in 55 leprosy patients…Of interest, indeterminate patterns were also found in a higher proportion of leprosy contacts (25/39; 64.1%), probably reflecting a high prevalence of subclinical M. leprae infection among leprosy contacts. More importantly, HIV-1 ELISA-negative sera from leprosy patients (85%) and their contacts (56.7%) had a much greater likelihood of a positive reaction on immunoblot than did that of normal individuals (2.5%), again suggesting a high rate if subclinical M. leprae infection among the contacts…sera from 63.6% of leprosy patients and 23% of their contacts were repeatedly positive for HIV-1 by ELISA”. Although they call all but two of their WB patterns (which they interpret as 2/55 leprosy patients being HIV infected, that is, 100% specific for HIV infection) as indeterminate (yet see above), in their discussion they wrote; “Despite a lower HIV-1 prevalence among leprosy patients and their contacts, we had a very high rate of HIV-1 false-positive ELISA and WB results…our observation of cross-reactivity…with HIV-1 antigens suggest that HIV-1 ELISA and WB results should be interpreted with caution when screening individuals infected with M. tuberculosis or other mycobacterial species. ELISA and WB may not be sufficient for HIV diagnosis in AIDS-endemic areas of Central Africa where the prevalence of mycobacterial diseases is quite high”.98

Since:

(i) mycobacterial infections are widespread in Africa;

(ii) the vast majority of the infected individuals and their contacts have “HIV-1 false-positive ELISA and WB results”;

tens of millions of Africans would be expected to have a positive HIV-1 antibody test even if not one African has ever been infected with HIV.

IMMUNE DEFICIENCY

The ‘AID’ in AIDS in an acronym for acquired immune deficiency, that is, a decrease in T4 cells. The ‘S’ stands for a syndrome of diseases whose number has been increased on three occasions since 1982. According to the HIV theory of AIDS, HIV kills T4 lymphocytes, that is, HIV induces immune deficiency which in turn leads to the appearance of the diseases constituting the clinical syndrome.

AIDS researchers in Africa, including those from the CDC and the WHO admit that immune deficiency in Africa has existed for a considerable time and has not been due to HIV. “Tuberculosis, protein calorie malnutrition, and various parasitic diseases can all be associated with depression of cellular immunity”.99 “A wide range of prevalent [in Africa] protozoal and helminthic infections have been reported to induce immunodeficiency”100 and “…among healthy Africans resident in a non-AIDS area, the numbers of helper and suppressor lymphocytes were the same in HTLV-III/LAV [HIV] sero-positive and sero-negative subjects”.101 “Africans are frequently exposed, due to hygienic conditions and other factors, to a wide variety of viruses, including cytomegalovirus (CMV), Epstein-Barr virus (EBV), hepatitis B virus, and herpes simplex virus, all of which are known to modulate the immune system…Furthermore, the Africans in the present study are at an additional risk for immunologic alterations since they are frequently afflicted with a wide variety of diseases, such as malaria, trypanosomiasis, and filariasis, that are also known to have a major effect on the immune system”.102

According to Essex and his colleagues their “ELISA and WB results suggest that HIV-1 cross-reacting sera may contain antibodies that bind to HIV-1 proteins either on ELISA or on nitrocellulose membranes. M. leprae may have this potential, since the disease it causes is associated with an immunodeficiency that resembles HIV-1 in several respects. In addition, the immune dysregulation induced by M. leprae is often accompanied by the production of autoantibodies to numerous cellular proteins”. 98 “Patients who have malaria have severe immunoregulatory disturbances including decrease in T cells”. A significant number of these patients also test positive for HIV but they do not develop the AID clinical syndrome, leading Volsky et al to conclude, “exposure to HTLV-III/LAV or the related retrovirus and the occurrence of severe immunoregulatory disturbances may not be sufficient for the induction of AIDS”.97 “According to Canadian researchers, “In tuberculosis as well as in lepromatous leprosy, an immunosuppressive state will frequently develop in the host. This state is characterised by T lymphopenia with a decreased number of T helper [T4] cells and an inverted T-helper/T-suppressor cell ratio…immunosuppression induced by the infection with M. tuberculosis can persist for life, even when tuberculosis is not progressive”.103

One of the principal major signs of the Bangui definition of AIDS in Africa is loss of body weight. However, in a study of Rwandan women, over a 24 month period beginning in 1988, it was reported that nutritional status assessed by loss of body weight “was a significant predictor of eventual HIV seroconversion. Subsequent seroconvertors lost an average of 1.5 kg during the six months of the study compared with 1.0 kg gain (p = 0.001) for non-converters. Nine of 27 (33%) seroconvertors., compared with one of 44 (2%) controls, lost at least 5 kg in the 6 month period beginning one year before seroconversion….In addition to those findings for measured weight loss during follow-up, reported weight loss before enrolment was also a risk factor for subsequent seroconversion”.104 In other words, weight loss preceded the appearance of a positive antibody test by many months or even years, not vice versa, as the HIV theory of AIDS requires.

THE SYNDROME

The first definition of AIDS was put forward by the CDC in 1982. Between 1982-85, the syndrome (S) consisted mainly of two diseases, Kaposis sarcoma (KS) and Pneumocystis carinii pneumonia. None of the diseases which signified AIDS were new but, with one exception, they were previously rare. The exception was KS in Africa. This disease was present in high frequency including an aggressive form in eastern equatorial Africa long before the AIDS era.105 Extensive investigations before the AIDS era did not provide any evidence to suggest that:

a) KS was sexually transmitted;

b) the cause of KS was an infectious agent

By the middle of the 1980s the number of HIV infections as well as the number of AIDS cases especially those with KS, were in decline.8, 106 However, during the last quarter of 1984, and at the time that HIV was accepted as the cause of AIDS, AIDS was redefined by the addition of “mild and moderate diseases”. These included non-Hodgkin’s lymphoma and lymphoma limited to the brain. In 1987 the CDC redefined AIDS a second time introducing twelve new diseases including extrapulmonary (but not pulmonary) tuberculosis. The 1987 definition, which came into effect on September 1st, permitted so many degrees of freedom that nearly any sick individual, especially one belonging to a “risk group”, could be reported as an AIDS case.107 The 1987 definition led to an increase of AIDS cases which continued over a number of years. For example, four months after its introduction one institution reported a 19% increase in cases but “Because of the potential lag between publication of the new definition and its widespread use”, 19%, “may be an underestimate” of the true impact of the new definition.108

Despite the new definition, by 1990 the reported AIDS cases had again leveled and were again in decline.109 However, in 1993 AIDS was redefined yet again. The new definition retained the twenty three AIDS indicator diseases belonging to the 1987 definition and added three more: “pulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer”. In addition, for the first time, any individual was regarded as a case of AIDS solely with laboratory abnormalities, that is, seropositive with a T4 cell count less than 200/uL.110 According to a CDC report February 3, 1995, in the USA in 1994 there were a total of 80,691 cases reported to the CDC, “…which followed the 106,618 cases reported in 1993. The number of cases reported in each of these years was greater than that reported in 1992 (47,572) and followed the expansion of the AIDS surveillance case definition for adolescents and adults implemented on January 1, 1993…”. In other words by 1994 the reported AIDS cases started to decrease again. Furthermore of 79,674 cases reported among adolescents and adults in that year “…43,226 (54%) was reported based on the reporting criteria added to the definition in 1993. Of these, 39,513 (91%) persons had severe human immunodeficiency virus (HIV)-related immunodeficiency only (ie., less than 200 CD4+ T-lymphocytes per uL or a CD4+ T-lymphocyte percentage of total lymphocytes less than 14), 2357 (5%) had pulmonary tuberculosis (tuberculosis), 1239 (3%) had recurrent pneumonia, and 164 (less than 1%) had invasive cervical cancer; 47 persons were reported with greater than or equal to 2 of these clinical diseases. Of the 3713 persons reported with one of the three opportunistic illnesses (ie., pulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer), 1097 (30%) were women, 2237 (60%) were black, and 1785 (48%) were injection drug users…of the 1017 children, 50% were female, most were black (62%) or Hispanic (23%)”.111

Although AIDS again began to decrease 1994, most of the HIV experts claim that the decline commenced in 1996, and coincided with the introduction of a new drug treatment known as Highly Active Anti-Retroviral Therapy (HAART) and thus is the result of HAART. Such a claim can be accepted only by prospective, double-blind controlled studies but no such studies exist. The claim that the decrease began in 1996 and is due to HAART is not even accepted by all HIV/AIDS experts. According to George Lemp and his colleagues from the AIDS Office, San Francisco Department of Public Health, the annual number of infections peaked in 1982 and the annual number of AIDS cases in 1992. “The decline in the incidence of AIDS in San Francisco reflects the dramatic reductions in new HIV infections that occurred a decade previously and that were achieved as a result of significant changes in high-risk behaviors, primarily among homosexual and bisexual men. Changes in HIV seroincidence must be factored in before attributing the decrease in AIDS incidence to more effective combination antiretoviral treatment”.112 In fact at present evidence exists which shows that despite its name, HAART, such drug combinations have no anti-retroviral effect. By design, the effect of all the drugs used in HAART is to decrease the HIV DNA. However, although many have tried, to date nobody has found proof of such an effect. Such proof is not found even in one of the latest publications.113, 114 In fact, Italian researchers reported an increase of HIV DNA following HAART, an observation totally at odds with their presumed anti-HIV effect.115 Although the possibility cannot be excluded that HAART may possess a clinical effect independent of HIV, this does not seem to be the case. In a study conducted by Michael Gottlieb and his associates it was shown that after 18 months on HAART, 26% of patients had developed AIDS which is a much higher rate than the 2% of patients not taking anti-retroviral treatment.14, 116, 117

Although in the popular press one hears/ reads of a Lazarus-like effect of HAART, such enthusiasm is not shared by the physicians responsible for prescribing these drugs. “As physicians venture into even wilder frontiers of HIV treatment, the grand experiment with combination therapies, called Highly Active Anti-Retroviral Therapy, or HAART, is rushing forward without any data. No-one is keeping track”.118 Apparently one of the few physicians, if not the only one who tries to make any sense of HAART is Michael Saag who supervises research and the care of more than one thousand AIDS patients in Birmingham, Alabama. “In one year, 157 of Saag’s patients collectively took 189 different drug formulas, with only three patients taking the same mix of HAART drugs…despite such rigorous, individualized medical attention, Saag says, the HAART “’dam’ is already leaking and there’s high danger of it collapsing altogether…Failures are occurring right and left…We don’t know what we are doing. Hubris! Hubris! We need to be scientists every step of the way and do our darndest to seek what reality is”.118 According to Dr Wafaa El-Sadr from Harlem Hospital “it takes a heap of denial to reach anything but sobering, even grim conclusions” regarding HAART.118

The first reports of AIDS in Africa were published in 1984,99, 119 and one year later there was an official definition of AIDS in Africa. However, what is called AIDS in Africa is almost unrecognisable as AIDS in the West, so much so that if African patients switched continents, very few would remain AIDS cases. This is due to the existence of two completely different AIDS definitions, one applying to Africa and the other to the rest of the World (except Asia and Latin America). Unlike the AIDS definition in the West, the 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, diarrhoea, cough and fever120 (see Appendix). These are common and non-specific manifestations of many diseases which are endemic in Africa and were so, long before the AIDS era. This is accepted by some of the best known AIDS researchers including those from Belgium, the WHO and the CDC. According to a former director of the WHO Global AIDS program, “…recognition of paediatric AIDS is particularly difficult in Kinshasha [Zaire], since many children have severe infant and childhood diseases with similar manifestations (eg. weight loss, chronic diarrhoea)”.90 Anthony Fauci, Director of the National Institute of Allergy and Infectious Diseases in the USA, discussing the AIDS definition in Africa, states: “Well, of course it will be less reliable (than that used in non-Third-World countries). One typical example is what we call ‘slim disease’. It’s a wasting syndrome seen in Africa. Now that wouldn’t fall under any categorizataion of AIDS by the standard empirical definition, but nevertheless, (slim disease) is being considered AIDS in Africa” (AIDS Alert, January 1987). According to Myron Essex, on whose work speculations as to the African origin of HIV is mainly based, “…malnutrition and general lack of medical services contributed to diarrhoea, tuberculosis, and other common African diseases that signify AIDS” (New Scientist, 18 February 1988).

Furthermore, no correlation exists between AIDS and HIV seropositivity in Africa. In one study, 83% of patients with suspected AIDS were HIV positive, but so were 44% with malaria, 97% with herpes zoster, 43% with pneumonia, 67% with amoebic dysentery and 41% with carcinoma.121 In the other study, 42% of women with recurrent abortions, 67% with vaginal ulcerations and 33% with haemorrhoids had a positive HIV antibody test. While the Bangui AIDS definition had a positive predictive value for HIV seropositivity of 62% in one of the studies and 83% in the other, in the same studies the positive predictive value of amenorrhoea was 42% and 89% respectively.122 In a 1990 study conducted by de Cock and his associates, 698 adult corpses were examined and had serological tests. Deaths were considered due to “AIDS” if the corpses had physical signs satisfying the Bangui African AIDS definition, or if the diagnosis before death was “AIDS, retroviral disease, wasting, pneumonia, chronic diarrhoea, extrapulmonary tuberculosis”. (Although pulmonary tuberculosis was not an AIDS indicator disease in 1990 nonetheless, on this basis, the researchers claimed underestimation of the number of “AIDS” cases). Under this guise, AIDS was the cause of death in 16 per cent of male and 15 per cent of female corpses. Overall, 43 per cent of all males and 34 per cent of all females with and without “AIDS” had a positive Western blot test. Of the “AIDS” cases, only 65 per cent had a positive test.123

Although an individual from the “Western industrialised” countries with symptoms which constitute AIDS in Africa is not considered an AIDS case, the converse is not true. Any African with the AIDS indicator diseases of the 1987 or 1993 CDC AIDS definition, even if not tested for T4 cells or HIV antibodies, is considered to have AIDS. According to a Lancet editorial,124 the developing world “bears more than 90% of the global burden of HIV infection” and that “Tuberculosis is the leading cause of death worldwide among people with HIV”. And one of the most eminent experts on HIV/AIDS in Africa, De Cock, and his associates, state that the prevalent cases of tuberculosis in the developing World is 12-16 million; annual incidence of tuberculosis is 3.5-10.7 million and the annual deaths 1.14-3.96 million. In sub-Sahara Africa these numbers are 2- 3; 0.66-1.66 and 0.27-0.79 million respectively.125 Since:

(a} the vast majority of tuberculosis cases are expected to have a positive HIV antibody test even if not infected;

(b) patients with tuberculosis may have abnormally low numbers of T4 cells, that is, they have AID;

it follows then, that millions of Africans would have AIDS even if no one of them is infected with HIV. Furthermore if these patients are treated with antiretroviral drugs for HIV instead of tuberculosis then such treatment will be more costly but ineffective.

CONCLUSION

A credible theory retroviral theory of AIDS must explain and predict all data including that on sexual transmission . From a review of the epidemiological data pertaining to HIV/AIDS and sexual activity, unless we accept that HIV is able to discriminate between individuals on the basis of sexual preference or race, we must conclude that although HIV/AIDS may be sexually acquired, it is not a sexually transmitted disease.

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