World Journal of Microbiology & Biotechnology
(1995) 11, 135-143
AIDS in Africa: distinguishing fact and fiction
E. Papadopulos-Eleopulos (1) Valendar F.Turner (2) John M. Papadimitriou
(3) Harvey Bialy (4)
(1) Corresponding author, Department of Medical Physics,
The Royal Perth Hospital, Perth 6000 Western Australia; (2) Department
of Emergency Medicine, Royal Perth Hospital; (3) Department of Pathology,
University of Western Australia; (4) Bio/Technology 65 Bleeker St. New
York, NY 10012 USA.
The data widely purporting to show the existence and heterosexual
transmission in Africa of a new syndrome caused by a retrovirus which induces
immune deficiency is critically evaluated. It is concluded that both acquired
immune deficiency (AID) and the symptoms and diseases which constitute
the clinical syndrome (S) are long standing in Africa, affect both sexes
equally and are caused by factors other than HIV. The presence of positive
HIV serology in Africans represents no more than cross-reactivity caused
by an abundance of antibodies induced by the numerous infectious and parasitic
diseases which are endemic in Africa, that is, a positive HIV antibody
test does not prove HIV infection. Given the above, one would expect to
find a high prevalence of "AIDS" and "HIV" antibodies
in Africa. This is not proof of heterosexual transmission of either HIV
Following the appearance in the West in the early 1980s of AIDS in gay
men, many European and American researchers looked for AIDS in Africa.
There were three reasons for this. One was Dr. Robert Gallo's hypothesis
that AIDS is caused by a retrovirus HTLV-I, or a similar virus. (At the
time it was known that Africans had a high prevalence of positive HTLV-I
serology). The other reasons were the high prevalence of Kaposi's sarcoma
(KS) in Africa, and the diagnosis of "AIDS" in a small number
of patients of African origin who were living in Europe. Yet, there were
so many problems with the HTLV-I theory of AIDS that by 1984 it had been
abandoned, even by Gallo himself, and although KS was practically non-existent
in gay men before the AIDS era, KS has been present in Africa since antiquity.
Its characteristic clinical appearances are described in the Ebers papyrus
which dates from 1600 B.C. As for the AIDS cases described by Belgian doctors
in the patients of African descent, the doctors who reported these cases
did not exclude the possibility that AIDS has always been present in Africa
(Clumeck et al., 1984). Despite these facts, the claim that the cause of
AIDS everywhere, including Africa is HIV, has been overwhelmingly accepted.
In fact, AIDS in Africa became of such pivotal significance to the HIV/AIDS
theory that in 1990 nearly 600 "AIDS-related" studies were conducted
in Africa. Yet even up to 1994, "There have been few studies of the
impact of HIV-1 infection on mortality in Africa, and none for a general
rural population" (Mulder et al., 1994). In this widely publicized
report, which appeared in the Lancet, Mulder and his colleagues tested
blood samples from Ugandan rural subsistence farmers for "HIV-1 antibodies
at the Uganda Virus Research Institute". Of 9389 individuals tested,
4.8% were found to be positive. "Deaths were ascertained over 2 years"
and 198 were recorded. Of these 109 were in seronegative individuals and
89 in seropositive individuals. Of the latter, 73 were adults. In a commentary
accompanying publication of this study, researchers from the CDC wrote:
"An ironic feature of this work is that it does not require a belief
that HIV is the cause of AIDS. Rather, the study shows that the simple
finding of antibodies against HIV in an individual's serum predicts a likelihood
of death within the next several years far above that for a seronegative
individual. Although most reasonable observers do accept that HIV causes
AIDS, even sceptics cannot fail to acknowledge the high prevalence of antibody
to HIV in Africa. If there are any left who will not even accept that antibody
to HIV indicates infection with the virus, their explanation of how HIV
seropositivity leads to early death must be curious indeed" (Dondero
& Curran, 1994). In the following we present just such an alternative
explanation of this, and other published studies on the "epidemic"
of AIDS in sub-Saharan Africa. We leave it to the reader to judge exactly
how curious it is.
Acquired Immune Deficiency (AID)
AIDS researchers in Africa, including those from the CDC and WHO, admit
that immune deficiency in Africa has existed for a considerable time and
this has not been due to HIV. "Tuberculosis, protein calorie malnutrition,
and various parasitic diseases can all be associated with depression of
cellular immunity" (Piot et al., 1984). "A wide range of prevalent
[in Africa] protozoal and helminthic infections have been reported to induce
immunodeficiency" (Clumeck et al., 1984). "...among healthy Africans
resident in a non-AIDS area, the numbers of helper and suppressor lymphocytes
were the same in HTLV-III/LAV seropositive and seronegative subjects..."
(Biggar, 1986). "Africans are frequently exposed, due to hygenic conditions
and other factors, to a wide variety of viruses, including CMV, EBV, hepatitis
B virus, and HSV, 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" [CMV=cytomegalovirus;
EBV=Epstein-Barr virus; HSV=herpes simplex virus] (Quinn et al., 1987).
The Syndrome (S)
If AIDS in Africa is the same condition with the same cause as anywhere
else in the world then AIDS in Africa and AIDS in the West should be identical.
This is not the case and what is called AIDS in Africa is almost unrecognizably
different from AIDS in the West, so much so that if African patients suddenly
switched continents, very few Africans would remain AIDS cases. This is
due to the existence of multiple AIDS definitions, one for Africa (the
same for adults and children), one for adults in North America, Europe
and Australia, one for children in these countries and one for Latin America.
Unlike the AIDS definition in the West, the WHO Bangui definition for Africa
does not require immunological (T4 lymphocyte cell or antibody) tests or
a specific disease diagnosis but consists largely of symptoms such as weight
loss, diarrhoea, cough and fever. For example, an African with diarrhoea,
fever and persistent cough for longer than one month is, by definition,
an AIDS case. However, the symptoms listed in the Bangui definition (WHO,
1986) are common and non-specific manifestations of many diseases which
are endemic in Africa and were so long before the AIDS era. This is accepted
by some of the best known AIDS researchers including those from Belgium,
the WHO and the CDC. According to Jonathan Mann, former director of the
WHO Global AIDS program, and his colleagues, "...recognition of pediatric
AIDS is particularly difficult in Kinshasha [Zaire], since many children
have severe infant and childhood diseases with similar manifestations (eg,
weight loss, chronic diarrhoea)" (Mann et al., 1986). Anthony Fauci,
Director of the National Institute of Allergy and Infectious Diseases in
the United States, 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 categorization of AIDS
by the standard empiric definition, but nevertheless, (slim disease) is
being considered AIDS in Africa" (AIDS Alert, January 1987). According
to Myron Essex on who's 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, 18th February 1988).
In summary, although, the best known researchers of African AIDS clearly
accept that both AID and the AID syndrome (S) existed in Africa long before
the AIDS era and that they were caused by agents other than HIV, the same
researchers expect the world to accept that in Africa there is a new disease,
AIDS, caused by a new virus, HIV.
Antibody Tests for HIV
The evidence for the existence of HIV in Africa is based on the random
testing of Africans for the presence of HIV antibodies. The HIV antibody
tests rely on the presence or absence of reactions between antibodies present
in patients' blood and certain proteins which are believed to be unique
to HIV. Even if the proteins are proven to unique to HIV, which at present
is not the case, a positive test cannot be considered proof of HIV infection.
This is because non-HIV antibodies can (and do, see below) react with the
"HIV proteins" producing positive tests in individuals who are
not HIV infected. Because of this, before the test is used to diagnose
HIV infection the test's specificity must be determined, one must determine
how often false-positive tests occur. For this one must:
A thorough search of the HIV antibody test literature fails to show
a single instance of the use of the above, the only scientifically valid
method of determining the specificity of the HIV (or any) antibody tests.
Indeed, comparisons between the published work on retrovirology and the
presently worldwide data on HIV reveals that no researcher has yet met
the requirements for an HIV gold standard. This is because the phenomena
collectively inferred as HIV (reverse transcriptase, virus-like particles,
"HIV antigens", and "HIV PCR"), are all non-specific
(Papadopulos-Eleopulos et al., 1993a, 1993b). The lack of a gold standard
has already been adduced by one of the best known HIV/AIDS researchers,
William Blattner: "One difficulty in assessing the specificity and
sensitivity of retrovirus assays is the absence of a final 'gold standard'.
In the absence of gold standards for both HTLV-I and HIV-1, the true sensitivity
and specificity for the detection of viral antibodies remain imprecise"
(Blattner, 1989). For some unknown reason, HIV experts (such as Mulder)
determine the specificity of the HIV antibody tests by repeating an antibody
test or a combination of antibody tests an arbitrary number of times and
use another antibody test as a gold standard. This was the method used
by Burke and his colleagues and many HIV/AIDS experts, including David
Ascher, believe this data shows the false-positive rate of the HIV antibody
tests to be 1/1,000,000 (Weiss & Thier, 1988; Ascher & Roberts,
1993). According to Mulder and colleagues, their "HIV testing algorithm
had a sensitivity and specificity of close to 100%". Mulder's algorithm
(Nunn et al., 1993) is a far less substantial version of Burke's algorithm
and, like Burke's, uses the Western blot as a gold standard. For them,
the true serostatus depends on repeating two different ELISAs until they
are concordant, an outcome which could eventuate by making the same mistake
twice. A positive ELISA followed by a positive WB is also regarded as proof
of HIV infection. However, it is not possible to determine the specificity
of an HIV antibody test by repeating the test, or using combinations of
the same and other antibody tests as Burke and Mulder and many others have
done. According to Philip Mortimer, director of the Virus Reference Laboratory
of the Public Health Laboratory Service, London, UK: "Diagnosis of
HIV infection is based almost entirely on detection of antibodies to HIV,
but there can be misleading cross-reactions between HIV-1 antigens and
antibodies formed against other antigens, and these may lead to false-positive
reactions. Thus, it may be impossible to relate an antibody response specifically
to HIV-1 infection. In the presence of clinical and/or epidemiological
features of HIV-1 infection there is often little doubt, but anti-HIV-1
may still be due to infection with related retroviruses (e.g. HIV-2) which,
though also associated with AIDS, are different viruses" [italics
ours] (Mortimer, 1989). Although Mortimer et al. (1985) as well as Gallo
and his colleagues (Weiss et al., 1985) used clinical and/or epidemiological
features" to determine the specificity of the HIV antibody tests,
this in scientifically invalid. The use of clinical and/or epidemiological
features is not a gold standard for the presence or absence of a retrovirus
and use of such a scheme creates many problems. For example, because the
vast majority of positive tests occur in individuals who are asymptomatic,
the vast majority of positive tests must be construed as false-positives.
Mulder et al had 377 individuals with a positive test. Of these, 89 died
within 2 years. Although not stated, we can assume that many of the remaining
HIV positive cases were asymptomatic and thus, according to Mortimer, all
these individuals had false-positive tests. Of the 73 adults who died,
only 5 had "AIDS"! the other 68 died of unlisted causes and if
asymptomatic for "AIDS" must all be regarded as false-positive
Epidemiological data show that AIDS patients in general and Africans
including healthy Africans have high levels of antibodies. For example,
United States data indicates that serum IgG levels are higher in HIV+ American
Blacks (mean 2234 ñ 930 mg/dl) than in HIV+ Caucasians (mean 1601
ñ 520 mg/dl). Serum IgG levels are also higher in Black blood donors
(mean 1356 ñ 220 mg/dl) than in Caucasians (mean 1072 ñ 243
mg/dl) (Lucey et al., 1991). Thus, in these individuals with high level
of antibodies one must expect cross-reactions with HIV antigens to be the
rule rather than the exception. That this is the case is amply demonstrated
by the African evidence and in fact is accepted by the best known expert
on African HIV/AIDS. In 1986, Quinn, Mann, Curran and Piot wrote, in Africa
"...serodiagnosis is complicated by the need for confirmatory testing
because of the presence of possible cross-reacting antibodies" (Quinn
et al., 1986). One year earlier Biggar stated that "...reactivity
in both ELISA and Western blot analysis may be non-specific in Africans...the
cause of the non-specificity needs to be clarified in order to determine
how they might affect the seroepidemiology of retroviruses in areas other
than Africa, such as the Caribbean and Japan...Serological studies from
Africa would need to be re-evaluated with a more specific test before conclusions
can be drawn" (Biggar et al., 1985). Other eminent HIV/AIDS researchers
including Weiss accepted that African sera "may give a false-positive
result on direct binding assay systems, or on western blots" (Serwadda
et al., 1985). Not only are positive HIV antibody tests in Africa considered
proof of HIV infection, without any re-evaluation the criteria used for
a positive test are far less stringent than those used in the West. However,
this year no less a person than Myron Essex and his colleagues presented
unambiguous evidence that both ELISA and WB may not be specific in Africa.
Essex and his colleagues reported that "...leprosy patients and their
contacts show an unexpectedly high rate of false-positive reactivity of
HIV-1 proteins on both WB and ELISA". The cross-reactivity was found
to be caused by antibodies directed against two major carbohydrate-containing
M. leprae antigens--phenolic glycolipid I and especially lipoarabinomannan,
an arabinose-containing lipopolysaccharide which is also present in M.
tuberculosis and other mycobacteria. They warned, "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" (Kashala
et al., 1994). Cross-reactivity of antibodies to mannans with "HIV
proteins" was also reported by Muller and colleagues who found, "Polyclonal
antibodies to mannan from yeast also recognize the carbohydrate structure
of gp120 of the AIDS virus" (Muller et al., 1990). Others have "shown
that normal human serum contains antibodies capable of recognizing the
carbohydrate moiety of the HIV envelope glycoproteins", gp41, gp120
and gp160 (Tomiyama et al., 1991). In 1986, Mann and colleagues reported
that in a tuberculosis santitorium in Kinshasa, Zaire, half of the suspected
pulmonary cases, one third of the confirmed cases and two thirds of the
confirmed extra-pulmonary cases had a positive HIV Western blot antibody
test (Nzilambi et al., 1986). Tuberculosis (TB), the cause of which is
a mycobacterium, is endemic in Africa. Of the 661 million people in sub-Saharan
Africa, 2-3 million have active TB with an annual mortality of 790,000.
Despite this and the fact that in adults, "HIV infection" usually
follows TB infection, TB has now become an AIDS defining illness, indeed
30-50% of African "AIDS" deaths are from TB. It is of great significance
that although neither the Mulder paper nor the commentary on it elaborated
on the causes of death in the 5 "AIDS" cases, the authors of
the latter wrote, "More information is needed to clarify how many
of the excess deaths could have been delayed through optimum medical prevention
and therapy of such HIV-associated illnesses as tuberculosis, other pneumonias,
and diarrhoeal disease". However, since:
Thus, those "who will not even accept that antibody to HIV indicates
infection with the virus" have no need to postulate a "curious"
or even a novel explanation for the relationship between "a positive
HIV antibody test" and AIDS, or between positive HIV serology and
mortality. In fact, Mulder's data does nothing more than prove their predictions
(Papadopulos-Eleopulos et al., 1993a). Indeed, non-specific antigen/antibody
reactions are frequently exploited in clinical practice. For example:
HIV and AIDS
In 1984, in the first ever published paper describing HIV antibody testing
of Africans, Montagnier and his colleagues wrote, "The prediction
that a single infectious agent is at the origin of AIDS implies that all
those with proven AIDS show signs of infection" (Brun-Vezinet et al.,
1984). The presence of HIV in all AIDS patients is a necessary condition
but is not sufficient proof that the virus is the cause of AIDS. Correlation
is not proof of causation (Duesberg, 1989). Ninety eight percent of haemophiliacs
with AIDS test positive for the presence of hepatitis B virus (Brenner
et al., 1991), in fact hepatitis B virus (HBV) seropositivity is a predictor
for HIV seropositivity, but no one claims that HBV is the cause of AIDS.
No such degree of 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. 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
(Widy-Wirski et al., 1988; Strecker et al., 1993).
One of the principal major signs of the Bangui definition is loss of
body weight. However, in a study of Rwandan women over a 24 months 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 nonconvertors. Nine
of 27 (33%) seroconvertors, compared with one of 44 (2%) controls, lost
at least 5Kg in the 6-month period beginning 1 year before their 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"
(Moore et al., 1993). In other words, this study found that weight loss
preceded HIV seroconversion by many months or even years. According to
Myron Essex, "The more medical scientists research the AIDS epidemic
in Africa, the more confusing the picture becomes...Among 37 people in
Ivory Coast, West Africa, with symptoms of AIDS, as defined by the World
Health Organization, 13 [35%] did not appear to have antibodies to HIV-1
or HIV-2, the second AIDS virus discovered more recently. A similar study
in Sengal uncovered 16 of 44 [36%] patients with AIDS, who again showed
no sign of infection with either virus" (New Scientist 18/2/88 page
27). Thus the HIV hypothesis of AIDS does not satisfy even the most fundamental
criterion for proof of an aetiologic agent. More extensive, and thoroughly
referenced critiques of its numerous deficiencies can be found in (Duesberg,
1992; Papadopulos-Eleopulos et al., 1992a, 1992b, 1993a, 1993b, 1994).
"To evaluate acquired immunodeficiency syndrome (AIDS) in central
Africa a prospective study was done in Kigali, Rwanda, where Kaposi's sarcoma
(KS) is endemic". The study was conducted by researchers from Belgium,
the Netherlands and Rwanda (Van De Perre et al., 1984). In 1983, these
workers "sent a questionnaire to all clinicians at the Centre Hospitalier
de Kigali asking them to make a special note over a 4 week period of new
patients who had clinical evidence of opportunistic infection (OI) and/or
generalised or multifocal Kaposi's sarcoma (KS) or who had the AIDS prodrome.
The prodrome [patients with the prodrome were ultimately classified as
AIDS patients] was defined by at least two of the following: loss of more
than 10% body weight, diarrhoea for at least 2 months with no pathogen
isolated, chronic fever of unknown origin lasting for at least 2 months,
and generalised lymphadenopathy consisting of palpable lymph nodes larger
than 1 cm at two or more extrainguinal sites for more than 3 months...Subsequently,
immunological evaluations were done in Kigali, after which we retained
as having AIDS or probable AIDS patients presenting with the above clinical
features provided they also had a decreased ratio of helper/inducer to
suppressor/cytotoxic T cells", that is a decreased T4/T8 ratio. They
found 26 such patients (17 males and 9 females), two of which were children.
"The 24 adult patients denied bisexuality or homosexuality or intravenous
drug use". Discussing their findings the authors wrote "The study
confirms that AIDS exists in Rwanda, a central African country east of
Zaire. The detection of 26 AIDS patients in a short period supports that
AIDS may be a public health problem in central Africa...Characteristically,
African AIDS affects women as well as men, a pattern very different from
the sex ratio (15:1) described in the chronic form of KS that has for many
years been seen in central Africa...The low sex ratio suggests that heterosexual
contact in the most frequent mode of transmission in central Africa".
In the same year and month, researchers from Belgium, Zaire, and the
USA including the CDC, searched for AIDS in Zaire. The authors stated that
"Because of limited diagnostic facilities we used a case definition
which included clinical features of AIDS and the immunological characteristics
of low T helper cell counts and low helper to suppressor ratios which have
been hallmarks of AIDS. We believe that this combination strengthens the
case definition in an area where severe infectious diseases abound, often
going undiagnosed". During a three week period they identified 38
such patients. Ten patients had "Chronic mucocutaneous HSV [herpes
simplex virus] infection", 14 bilateral interstitial pneumonia "with
severe dyspnoea, unresponsive to antibiotics or tuberculostatics",
31 oral and/or oesophageal candidiasis and 6 had disseminated KS. Regarding
the latter they wrote "Since KS has long been endemic in Zaire, only
patients with fulminant KS were included". Discussing their findings
they wrote: "Two important differences between AIDS in Zaire and the
disease in patients of European or American origin merit discussion-- namely,
the sex distribution and apparent lack of risk factors among patients in
Zaire...The essentially equal proportions of males and females would require
that transmission occurs both male to female and female to male, since
one-direction transmission would soon result in an imbalance in the ratio"
(Piot et al., 1984).
In 1984, sera from 37 out of the 38 patients who were diagnosed in Kinshasha
in October 1984 were tested for HIV antibodies by Montagnier and 19 of
his associates including researchers from the CDC. The sera were tested
by ELISA and followed by a RIPA (radioimmunoprecipitation assay, similar
to the Western blot). The latter was considered positive if a p24 band
was present. The p41 band and also a 84-kD band were not considered diagnostic
because "The 43-kD [p41] band and the 84-kD band are cellular contaminants
that are immunoprecipitated in all the tested sera", from both patients
and controls. (Yet today, in Africa, the p41 band on its own is considered
to represent a positive WB and thus proof of HIV infection). Thirty two
(88%) patients were positive by both tests. So were six out of 26 (23%)
controls. (Brun-Vezinet et al., 1984). However: (a) with the exception
of a few other reports from Africa (see below) no such correlation between
ELISA and WB has ever been reported. For example, Burke and his colleagues
tested 1.2 million healthy American military recruits and found that of
6000 individuals with two consecutive positive ELISAs, only 2000 subsequently
had a positive Western blot (Burke et al., 1988). In Russia, in 1991, of
30,000 positive screening ELISAs, only 66 were Western blot positive (Voevodin,
1992); (b) since 1987, nobody in the world with the possible exception
of Montagnier, considers the p24 band proof of HIV infection, not even
In July 1984, the research groups who reported the first 38 cases of
AIDS from Kinshasa started a new study in the same city. During an 8 month
period they had "565 suspected AIDS cases", that is, they had
565 cases which satisfied "At least one of the following three clinical
criteria: (a) A syndrome with profound weight loss (> 10% of normal
body weight) plus either chronic diarrhoea (lasting at least 2 mo) or chronic
fever and asthenia (lasting 1 + mo); (b) An opportunistic infection included
in the Centers for Disease Control definition of AIDS (restricted resources
limited recognized opportunistic infections to candidal esophagitis, cryptococcal
meningitis and chronic ulcerated herpes infection; and/or (c) Disseminated
Kaposi's sarcoma, with histopathologic evidence of visceral invasion".
Of the 565 patients, 332 (58.8%) were found to have a positive HIV antibody
test, and because of this were considered to be confirmed AIDS cases. "A
specimen was considered positive for antibody to HTLV-III if it was repeatedly
reactive on two separate ELISA assays ...The male-female ratio was 1:1.1.
Men with AIDS were significantly older than women... Nearly half of all
patients (145) were not married... Women with AIDS more likely than men
with AIDS to be unmarried". Commenting on their results the authors
"Several epidemiologic features of AIDS in Kinshasa should be noted.
A nearly equal sex distribution of cases has now been demonstrated in this
large series. This age distribution by sex, including a lower mean age
for female patients, is typical of sexually transmitted diseases. However,
interpreting surveillance data on possible means of exposure to AIDS is
difficult. For example, the finding that 61% of women with AIDS are unmarried
has been cited to support theories of heterosexual transmission. However,
61% of nearly 933 women working at Mama Yemo Hospital are also unmarried"
(Mann et al., 1986).
Like Montagnier and the CDC, Gallo and his associates also tested Africans
for HIV antibodies. Of 53 patients with AIDS, including the first 26 patients
reported from Rwanda, "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. "All blood donors were of good socioeconomic status".
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. In the
WB, "serum samples possessing reactivity to HTLV-III p41 and/or p24
were scored positive. Gallo and his associates concluded, "In Central
Africa, as previously noted, the occurrence of the syndrome in young to
middle-aged men and women suggests that heterosexual contact is probably
the predominant mode of transmission of the AIDS agent. Furthermore, among
the 24 adults with AIDS that we saw in Rwanda, 12 of the 17 men had contact
with prostitutes, and three of seven women were prostitutes" (Clumeck
et al., 1985). The claims in the above studies that: (a) Africans have
AIDS; (b) In Africa "Homosexuality, intravenous drug use and blood
transfusions did not appear to be risk factors"; (c) an approximately
equal number of male and females have AIDS, as well as a positive HIV antibody
test; are interpreted as proof that in Africa, HIV and AIDS is heterosexually
transmitted. Indeed, the perceived heterosexual spread of AIDS in Africa
underlies the belief that HIV and AIDS will eventually overtake the West.
But, "The mere absence of data to the contrary does not by itself
make the opposite assertion true; if it did, science would be a much simpler
thing. While it is true that in Africa the incidence of AIDS and infection
with [HIV] is nearly equal among men and women, we ought not automatically
assume that heterosexual transmission of the AIDS virus is likely here...parasitic
disease has been found repeatedly to be a risk factor for seropositivity
to the AIDS virus or AIDS itself in Africa and Venezuela" (Pearce,
Nancy Padian and her colleagues who to date have most thoroughly investigated
heterosexual transmission of HIV/AIDS wrote: "We question whether
the ratio of male-to-female cases in Africa necessarily supports the hypothesis
that AIDS is primarily spread in Africa by bidirectional heterosexual transmission"
(Padian & Pickering, 1986). The fact that equal numbers of men and
women have AIDS or antibodies to HIV does not prove that AIDS is heterosexually
spread. Many diseases such as influenza, pneumonia, tuberculosis and appendicitis
have an equal sex distribution but this is not construed as proof of heterosexual
transmission. To prove that AIDS is spread by sexual activity one must
study a large number of index cases, isolate HIV, prove it is the cause
of AIDS, trace the sexual contacts of these cases and then isolate the
same agent. To date, no reliable data of this type has ever been presented
either in Africa, or anywhere else. In fact, according to Dr. Harry Haverkos
from the US National Institute on Drug Abuse, "Sexual contact tracing,
the standard practice in public health to combat such sexually transmitted
diseases as gonorrhoea and syphilis, has been avoided for tracing of HIV-infected
persons. Health department personnel are concerned about possible discrimination
associated with AIDS, plus the fact that there is no cure for the disease"
(Haverkos & Edelman, 1988). As far as Africa is concerned, one must
note that "AIDS patients reported to the CDC are classified as HT
[heterosexual] if they (1) report heterosexual contact with a person with
HIV infection or at increased risk for HIV infection (US-born) or (2) were
born in countries where HT is a major route of transmission (non-US born)"
(Chamberland et al., 1988). This means that a man/woman born in Africa
can be said to have acquired AIDS by heterosexual contact even if his/her
partner were not proven to have "HIV infection", or even if he/she
never had sexual intercourse. Given the fact that the best known HIV/AIDS
experts on African AIDS admit that (a) what is known as AIDS in Africa
has been present for centuries and was equally common in men and women;
(b) a positive HIV antibody test may not be due to HIV antibodies but to
the presence of antibodies formed in response to malaria, tuberculosis,
leprosy and many parasitic diseases; one would predict that in Africa an
equal number of men and women will have "AIDS" and positive antibody
tests. To explain these observations one has no need to invoke the activity
of a virus called HIV. In fact, the theory that AIDS in Africa is transmitted
heterosexually creates more problems than it solves.
In 1986, Gallo and his colleagues wrote, "We found no evidence
that other [than receptive anal intercourse] forms of sexual activity,
contribute to the risk" of HIV seroconversion (Stevens et al., 1986).
In the West, the largest (thousands of cases) and most judiciously conducted
prospective epidemiological studies such as the Multicenter AIDS Cohort
Study (Kingsley et al., 1987) have proven beyond all reasonable doubt that
in gay men the only significant sexual act related to becoming HIV antibody
positive and progressing to AIDS is receptive anal intercourse. A minority
of the studies also report cases which suggest transmission by passive
orogenital sexual activity (Caceres & van Griensven, 1994). Similarly,
the largest and best conducted studies in heterosexuals including the European
Study Group (1989) have also shown that for women, the only practice leading
to an increased risk of becoming HIV antibody positive is anal intercourse.
Therefore, in non-African countries the only risk factor for the acquisition
of HIV antibodies is anal intercourse in the passive partner (male or female),
and if the only cause for the development of HIV antibodies is HIV infection
then one must conclude that in non-African countries HIV is unidirectionally
sexually transmitted. Thus, at least in non-African countries "HIV",
like pregnancy, can only be acquired by the passive sexual partner and
cannot be transmitted to the active partner. The unidirectional transmission
of "HIV" observed in the West is further supported by Nancy Padian's
prospective study of heterosexual couples where, from a cohort recruited
from 1985 to March 1991 involving 72 male partners of HIV infected women,
there was "one probable instance" of female-to-male transmission
(Padian et al., 1991). In the whole history of Medicine there has never
been an example of a sexually transmitted disease which is spread unidirectionally,
and certainly not one that is spread unidirectionally in one country and
bidirectionally in another. Indeed, given this and the other differences
between AIDS in the West and Africa it is necessary to postulate that HIV
must indeed possess features even more unique than those already attributed
to it. Since the only sexual behaviour risk factor for a gay man is receptive
anal intercourse, an exclusively active male partner is at no risk of infection
by his passive male partner. Yet if this same person travelled to Africa
and changed his sexual orientation, he would now be at risk of infection
by his passive female partner. Thus, HIV must be able to distinguish an
individual's sexual preference, gender and country of residence.
More rationally, one might choose to agree with those African physicians
and scientists including Richard and Rosalind Chirimuuta (Chirimuuta &
Chirimuuta, 1987) who believe that immunosuppression and certain symptoms
and diseases which constitute African AIDS have existed in Africa since
time immemorial. According to Professor P.A.K. Addy, Head of Clinical Microbiology
at the University of Science and Technology in Kumasi, Ghana "Europeans
and Americans came to Africa with prejudiced minds, so they are seeing
what they wanted to see...I've known for a long time that Aids is not a
crisis in Africa as the world is being made to understand. But in Africa
it is very difficult to stick your neck out and say certain things. The
West came out with those frightening statistics on Aids in Africa because
it was unaware of certain social and clinical conditions. In most of Africa,
infectious diseases, particularly parasitic infections, are common. And
there are other conditions that can easily compromise or affect one's immune
system" (Hodgkinson, 1994). In the words of Dr. Konotey-Ahulu from
the Cromwell Hospital in London, "Today, because of AIDS, it seems
that Africans are not allowed to die from these conditions [from which
they used to die before the AIDS era] any longer. ...Why do the world's
media appear to have conspired with some scientists to become so gratuitously
extravagant with the untruth?" (Konotey-Ahulu, 1987)
We would like to thank all our colleagues and especially
Richard Fox, Bruce Hedland-Thomas, David Causer, Gary James, Udo Schulenk,
Phil Johnson, John Lauritsen and the staff of the Royal Perth Hospital
Library and the clerical staff of the Department of Medical Physics. We
especially thank Charles Thomas and Neville Hodgkinson for their help and
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