THE AFRICAN AIDS EPIDEMIC:
New and Contagious - or - Old Under a New Name?
By Peter Duesberg
An infectious epidemic is typically diagnosed by scientists
and non-scientists by a sudden increase in morbidity and mortality
of a population. As a result the affected population declines
significantly, and a relatively immune population emerges.
The most readable modern description of such an epidemic is
Albert Camus' "The Plague".
Roy Anderson, professor of zoology at the Wellcome Trust
Centre for Epidemiology of Infectious Diseases in Oxford,
UK, provides a recent scientific description in a piece entitled
"The spread of HIV and sexual mixing patterns" (Anderson,
1996). According to Anderson, "The historical and epidemiological
literature abounds with accounts of infectious diseases invading
human communities and of their impact on social organization
and historical events. We typically think of a new epidemic
in a "virgin" population as something that arises suddenly,
sweeps through the population in a few months, and then wanes
and disappears. Indeed, the classical epidemic curve for many
respiratory or intestinal tract viral and bacterial infections
is bell-shaped, with an overall duration of a few months to
a year or so. Figure 4-1 illustrates a well-documented example,
the 1665 plague in London, believed to have killed about one-third
of the population in a few months."
The seasonal poliomyelitis epidemics from the days prior
to the polio vaccine, and the ever new, seasonal flu epidemics
are specific modern examples of viral epidemics.
All of these viral and microbial epidemics have the following
(i) They rise exponentially and then decline within weeks or months
as originally described by William Farr in the early 19th
century (Bregman & Langmuir, 1990). The rise reflects
the exponential spread of contagion and the fall reflects
the resulting natural vaccination or immunity of survivors.
(ii) The epidemics spread randomly ("heterosexually" in the words
of AIDS researchers) in the population.
(iii) The resulting infectious diseases are highly specific reflecting
the limited genetic information of the causative microbe.
As a consequence the viral diseases are typically more
specific than those caused by the more complex bacteria
or fungi. It is for this reason that the viruses and microbes
are typically named for the specific disease they cause.
For example influenza virus is called after the flu, polio
virus after the poliomyelitis, and hepatitis virus after
the liver disease it causes.
(iv) The microbial and particularly the viral epidemics are self-limiting
and thus typically seasonal, because they induce anti-microbial
and viral immunity and select also for genetically resistant
By contrast, the following are characteristics of
diseases caused by non-contagious, chemical or physical factors:
(i) They follow no specific time course, but one that is determined
by the dose and duration of exposure to the toxin.
(ii) They spread according to consumption or exposure to toxic agents,
but not exponentially.
(iii) They spread either non-randomly with occupational or lifestyle
factors, or randomly with environmental or nutritional
(iv) They range from relatively specific to unspecific depending
on the nature of the toxin.
(v) They are limited by discontinuation of intoxication, but not
self-limiting because they do not generate immunity.
For example, the American pellagra epidemic of the rural
South in the early decades of the 20th century lasted for
decades and no immunity emerged, until a vitamin B rich diet
proved to be the cure. And it did not spread to the industrial
North which had a diet rich in Vitamin B.
Similarly the rather unspecific American epidemic of lung
cancer-emphysema-heart disease-etc. rose steadily, not exponentially,
in the 1950s and has lasted now for over 50 years without
evidence for immunity.
It did not spread randomly in the population but was restricted
to smokers. And it is now slowly coming down as smoking slowly
declines (Greenlee et al.,2000).
Likewise the American and European AIDS epidemics:
(i) rose steadily, not exponentially,
(ii) were completely non-randomly biased 85% in favor of males,
(iii) have followed first the over-use of recreational drugs, and
then the extensive use of anti-AIDS-viral drugs (Duesberg
& Rasnick, 1998),
(iv) do not manifest in one or even just a few specific diseases
typical of microbial epidemics,
(v) do not spread to the general non-drug using population.
AIDS manifests in a bewildering spectrum of 30 non-specific,
heterogeneous diseases. This is consistent with the heterogeneity of
the causative toxins. There is no evidence for AIDS-immunity in 18 years,
but the American/European AIDS epidemics are now coming down slowly
as fewer people use recreational drugs (Duesberg & Rasnick, 1998).
The above summary indicates that American and European
AIDS epidemics exhibit the characteristics of diseases caused
by non-contagious, chemical or physical factors NOT viruses.
African AIDS in numbers
Now I will briefly analyze how African AIDS measures up with
"the historical and epidemiological literature" described
by Anderson and others (Fenner et al.,1974).
My analysis is based on statistical numbers from the World
Health Organization (WHO) in Geneva, the United Nations and
the U.S. Agency for International Development & the U.S. Census
According to the WHO's Weekly Epidemiological Records,
the whole continent of Africa has generated between 1991 and
1999 a rather steady yield of 60,000 to 90,000 AIDS cases
annually, on average about 75,000 (WHO's Weekly Epidemiological
Records since 1991).
Based on the last available data from South Africa, 8,976
cases were reported there between 1994 and 1996 by the WHO,
corresponding to about 4,500 cases per year (WHO's Weekly
Epidemiological Records 1998 and 1995).
The WHO does not report how many of these cases are deaths,
how many survive with, and how many recover from AIDS.
However, it is evident from the WHO data that the African
AIDS epidemic is not following the bell-shaped curve of an
exponential rise and subsequent sharp drop with immunity,
that are typical of infectious epidemics. Instead it drags
on like a nutritionally or environmentally caused disease
(Seligmann et al., 1984), that steadily affects, what appears
to be only a very small percentage of the African population.
Given a current African population of 616 million (United
Nations Environment Programme, June 15, 2000), and an average
of 75,000 African AIDS cases per year, it follows that only
0.012% of the African population is annually suffering or
dying from AIDS. Likewise only 0.01% of the South African
population was suffering from AIDS between 1994 and 1996,
based on the 4,500 annual cases and a population of approximately
44 million (US Agency for International Development, "HIV/AIDS
in the developing World", May 1999). This means that the new
African AIDS epidemic only represents a very small fraction
of normal African mortality.
Based on a current average life expectancy for Africa of
about 50 years (US Agency for International Development, "HIV/AIDS
in the developing World", May 1999), the annual mortality
of 616 million people is 12.3 million. Thus even if we assume
that all AIDS cases reported by the WHO are deaths, the African
AIDS epidemic represents only 75,000 out of 12,300,000 deaths
per year, or 0.6% of all African mortality. Thus African AIDS
is certainly not one of the historical microbial epidemics
described by Camus and Anderson (see above). Since no immunity
has emerged in over a decade, the restriction of African AIDS
to a relatively small fraction of the large reservoir of susceptible
people indicates non-contagious risk factors that are limited
to certain subsets of the African population.
In view of the very small share (0.6%) that the African AIDS
epidemic seems to hold on Africa's total mortality, the question
arises whether the mortality claimed for AIDS is in fact new
mortality, that can be distinguished from conventional mortality,
or whether it is a minor fraction of conventional mortality
under a new name.
To answer these questions we must try to distinguish African
AIDS diseases from conventional African diseases (i) clinically as well as
The long list of African AIDS diseases can not be clinically
distinguished from their conventional counterparts
According to the WHO's Bangui definition of AIDS (Widy-Wirski
et al., 1988; Fiala, 1998) and the "Anonymous AIDS Notification"
forms of the South African Department of Health, African
AIDS is not a specific clinical disease, but a battery of
previously known and thus totally unspecific diseases, for
(i) "weight loss over 10%,
(ii) chronic diarrhea for more than a month,
(iii) fever for more than a month,
(iv) persistent cough,
(v) generalized pruritic dermatitis,
(vi) recurrent herpes zoster (shingles),
(vi) candidiasis oral and pharyngeal,
(vii) chronic or persistent herpes,
(viii) cryptococcal meningitis,
(ix) Kaposi's sarcoma"
Since these diseases include the most common diseases in
Africa and in much of the rest of the world, it is impossible
to distinguish clinically African AIDS diseases from previously
known, and concurrently diagnosed, conventional African diseases.
Thus African AIDS is clinically unspecific, unlike microbial
diseases, but just like some nutritionally and chemically
caused diseases (see above).
African AIDS is too small to be detected statistically
against the background of normal African morbidity, mortality
and growth rates
We have already pointed out that it is almost impossible
to be certain about the existence of a new African AIDS epidemic
that claims only 0.6% of African mortality, particularly since
all AIDS defining diseases are profoundly conventional African
The same is true if we try to determine the effect of the
presumably new African AIDS epidemic on the current growth
rates of Africa. The annual population growth rates of Africa
have been between 2.4 and 2.8% per year since 1960 based on
the American Agency for International Development & the U.S.
Census Bureau's "HIV/AIDS in the Developing World" (U.S. Agency
for International Development & U.S. Census Bureau, Feb. &
May 1999) and the United Nations' "African population Database
Documentation" (United Nations Environment Programme, June
As a result of the high African growth rates, the population
of the whole African continent has grown from 274 million
in 1960, to 356 million in 1970, to 469 million in 1980, and
to 616 million in 1990 (United Nations Environment Programme,
June 15, 2000). By comparison the annual growth rate of the
US is only 1% and that of Europe is only 0.5% (USAID, Feb.
& May 1999).
Because of the numerical discrepancy between the relatively
high African growth rates (2.4 to 2.8%) and the small annual
deficits of these growth rates to be expected from AIDS mortality
(0.6%), an African AIDS epidemic can not be identified or
confirmed based on its effect on the high African growth rates.
In view of this, and the complete overlap between the complex
battery of diseases that define the AIDS epidemic and their
conventional counterparts, it appears that the presumably
new AIDS epidemic can be neither distinguished epidemiologically
nor clinically from conventional African diseases and mortality.
Deceptive reporting obscures analysis of African AIDS
To all of us who have been subjected to the American AIDS
rhetoric, and indeed the rhetoric of our first meeting in
Pretoria last May, about the "catastrophic dimensions" of
African AIDS (Washington Post, April 30, 2000), the healthy
African growth rates come as a big surprise. Take as an example
of this rhetoric President Clinton's recent designation of
AIDS as a "threat to US national security ... spurred by US
intelligence reports that looked at the pandemic's broadest
consequences, ... particularly Africa ... [and] projected
that a quarter of southern Africa's population is likely to
die of AIDS ..." (Washington Post, April 30, 2000).
In view of this rhetoric, it would appear that neither President
Clinton nor the "U.S. intelligence" are aware of information
available to the American Agency for International Development
& the U.S. Census Bureau. Indeed the USAID & Census Bureau
seem to have noticed the discrepancy between the facts and
the rhetoric and are trying to hide it - the possible reason
why "the largest demographic impact of AIDS" is cautiously
described either as just a relatively small reduction in "life
expectancy" or in expected population growth (not loss!):
"Differences in population size between the AIDS-adjusted
and the non-adjusted scenarios are often substantial ... By
the year 2010 ... South Africa will have 5.6 million fewer
people ..." than expected based on current growth rates ("HIV/AIDS
in the Developing World", U.S. Agency for International Development
& U.S. Census Bureau, May 1999). A "catastrophe" 10 years
down the road - and a "threat to U.S. national Security" now!
The alarming tone of WHO's joint United Nations Programme
on HIV/AIDS, "AIDS epidemic update: December 1999" (UNAIDS
December 1999), announcing that Africa had gained 23 million
"living with HIV/AIDS", because they are "estimated" carriers
of antibodies against HIV, since the "early 80s" (WHO, Weekly
Epidemiological Record 73, 373-380, 1998) is equally surprising
in view of information available to the agency. Neither the
WHO nor the United Nations point out that Africa had gained
147 million people during the same time in which the continent
was said to suffer from a new AIDS epidemic. Likewise, South
Africa has grown from 17 million to 37 million in 1990 (United
Nations Environment Programme, June 15, 2000), and to 44 million
now ("HIV/AIDS in the Developing World", U.S. Agency for International
Development & U.S. Census Bureau, May 1999). In the last decade
South Africa has also gained 4 million HIV-positive people
(A. Kinghorn & M. Steinberg, South African Department of Health,
undated document probably from 1998, provided at the Pretoria
meeting). Thus South Africa has gained 4 million HIV-positives
during the same decade in which it grew by 7 million people.
Moreover, although the 23 million "estimated" HIV-antibody
positives are said to be "living with HIV/AIDS" by the WHO,
the agency does not offer any evidence for morbidity or mortality
exceeding the modest numbers, ie. about 75,000 cases annually,
reported by the it's Weekly Epidemiological Records (see above).
The agency's estimates of HIV-positives are indeed just
"estimates", because according to the 1985-Bangui definition
of African AIDS as well as to the current "Anonymous AIDS
Notification" forms of the South African Department of Health
- no HIV tests are required for an AIDS diagnosis (Widy-Wirski
et al., 1988; Fiala, 1998).
In addition the WHO promotes the impression of a microbial
AIDS epidemic, by reporting African AIDS cases cumulatively
rather than annually (WHO's Weekly Epidemiological Records
since the beginning of the epidemic). This practice creates
the deceptive impression of an ever growing, almost exponential
epidemic, even if the annual incidence declines (Fiala, 1998).
It would follow that the estimated increases in African HIV
antibody (!)-positives do not correlate with decreases in
any African population. On the contrary, they correlate with
unprecedented simultaneous increases in the country's populations
- hardly the "catastrophe" imagined by the Washington Post
and propagated by the WHO and the American AIDS establishment.
But this deceptive AIDS propaganda biases a scientific analysis
of African AIDS by all those who are not aware of the facts.
(1) The African AIDS epidemic fails all criteria of a
microbial or viral epidemic:
(i) It is steady, i.e. about 75,000 cases per year since
the early 1990s, instead of growing exponentially into the
large reservoir of 617 million susceptible people, as would
be typical of a new viral or microbial epidemic;
(ii) It is not self-limiting via immunity within weeks or
months, as is typical of a microbial and particularly of a
viral disease. Instead it appears to maintain for years a
rather steady share of African morbidity and mortality.
(iii) It is clinically exceedingly heterogeneous totally
lacking any specificity of its own, unlike all conventional
viral and even bacterial diseases. In conclusion, the African
AIDS epidemic does not have even one of the specific characters
of a viral or microbial epidemic.
(2) Since the suspected African AIDS epidemic of an average
of 75,000 annual cases can neither be identified as a new
(i) clinically because of its total lack of a clinical identity,
(ii) numerically because of its small share of the total
African morbidity and because of undetectable effects on the
rapid growth of the African population,
the primary scientific task of our AIDS panel will now be
to determine whether there is in fact a new epidemic of AIDS
defining diseases in Africa, or whether a fraction normal
morbidity and mortality has been renamed AIDS. The answer
to this question would be the first order of business for
all AIDS prevention and treatment programs considered by President
Mbeki. To find this answer, I second the proposal from an
African AIDS researcher published 13 years ago, "Clinical
epidemiology, not [HIV] seroepidemiology, is the answer to
Africa's AIDS problem" (Konotey-Ahulu, 1987).
(3) The African statistics of AIDS and HIV antibody-positives
confirm Mbeki's suspicion about discrepancies between the
African and American AIDS epidemics (Mbeki's letter to
U.S. President Clinton, Washington Post, April 19, 2000):
In Africa 23 million HIV-positives generate per year 75,000
AIDS patients, ie. 1 AIDS case per 300 HIV-positives.
But in the US, 0.9 million HIV-positives (WHO, Weekly Epidemiological
Record 73, 373-380, 1998) now generate per year about 45,000
AIDS cases (Centers for Disease Control, 1999), ie. 1 AIDS
case per 20 HIV-positives.
Thus the AIDS risk of an American HIV-positive is about
15-times higher than that of an African! Since over 150,000
healthy (!) HIV-positive Americans are currently treated with
DNA chain-terminating and other anti-HIV drugs (Duesberg &
Rasnick, 1998), and since American HIV-positives have a 15-fold
higher AIDS risk than African HIV-positives, President Mbeki
must be warned about American advice on "treatments" of HIV-positives.
(4) The discrepancies between African AIDS and infectious
disease, and the discrepancies between the high AIDS risk
of American compared to African HIV-positives can both be
readily explained by the hypothesis that AIDS is caused
by non-contagious risk factors and that HIV is a harmless
passenger virus (Duesberg, 1996; Duesberg & Rasnick, 1998).
According to this hypothesis the African AIDS diseases
are generated by their conventional, widespread causes, malnutrition,
parasitic infections and poor sanitation as originally proposed
by leading AIDS researchers including Fauci, Seligmann et
al. (Seligmann et al., 1984).
This hypothesis also offers a simple explanation for the
"heterosexual" distribution of AIDS in the African people,
a question also asked by Mbeki in his letter to President
Clinton (see above). Malnutrition, parasitic infections and
poor sanitation do not discriminate between sexes. By contrast,
American AIDS would be caused by recreational drugs consumed
by millions and anti-HIV drugs prescribed to about 200,000
including 150,000 still healthy HIV-positives (Duesberg &
Rasnick, 1998). The non-random, 85%-male epidemiology of American
AIDS reflects the male prerogative on hard recreational drugs
(heroin, cocaine) and the wide-spread use of drugs as male
homosexual stimulants (Haverkos & Dougherty, 1988; Duesberg
& Rasnick, 1998).
In the light of this hypothesis the new epidemic of HIV-antibodies
would simply reflect a new epidemic of HIV-antibody testing,
introduced and inspired by new American biotechnology. This
technology was developed during the last 20 years for basic
research to detect the equivalents of biological needles in
a haystack, but not to "detect" the massive invasions of viruses
that are necessary to cause ALL conventional viral diseases
(Duesberg, 1992; Duesberg & Schwartz, 1992; Duesberg, 1996;
Mullis, 1996; Duesberg & Rasnick, 1998; Mullis, 1998). But
this technology is now faithfully but inappropriately used
by thousands of AIDS virus researchers and activists to detect
latent, ie. biochemically and biologically inactive HIV or
even just antibodies against it (Duesberg & Bialy, 1996)!
The same technology also provides job security for other virologists
and doctors searching for latent, and thus biologically inactive,
viruses as their preferred causes of Kaposi's sarcoma, cervical
cancer, leukemia, liver cancer, and rare neurological diseases
- without ever producing any public health benefits (Duesberg
& Schwartz, 1992).
(5) President Mbeki must also be warned about Dr. Joe Sonnabend's
answer to the president's question about the epidemiological
discrepancy between the "heterosexual" AIDS epidemic in Africa
and the non-random, 85%- male epidemic in the U.S. (Mbeki's
letter to U.S. President Clinton, Washington Post, April 19,
According to Sonnabend's hypothesis, Africans acquire HIV
heterosexually, because they simultaneously suffer from a
long list of diseases, including "tuberculosis, malaria, other
protozoal infections, bacterial diarrheal infections, pneumonia,
plasmodium, Leishmania" etc. However, the very low AIDS risk
of an African HIV-positive, compared to an American, calls
this hypothesis into question. If the Sonnabend-hypothesis
were correct, African HIV-positives should develop AIDS much
more readily than their American counterparts. But the opposite
is true. In fact according to Sonnabend most Africans should
already have AIDS by the time they pick up HIV "heterosexually".
Moreover, the Sonnabend-hypothesis does not resolve the discrepancy
between relatively high share of children from 0-14 years
in African AIDS, ie. 7%, compared to the 1% share of AIDS
by their American counterparts (WHO, Weekly Epidemiological
Record, vol. 49, pp381-384, 4 December 1998). According to
the WHO, "AIDS in children is an important phenomenon in many
African countries, whereas it is relatively rare in industrialized
Again AIDS in children is not compatible with "heterosexual
transmission of HIV" while suffering from Sonnabend's
bewildering list of diseases. But AIDS in children is very
compatible with malnutrition, parasitic infection and poor
sanitation. Therefore, President Mbeki must be warned against
treatment of these children with DNA chain-terminators and
other anti-HIV drugs as suggested by Sonnabend's hypothesis.
Above article was presented before the South African Presidential
AIDS Advisory Panel.
Acknowledgment: I thank Charles Geshekter, professor of history,
Cal State University Chico, Chico, California for advice and
critical statistics (see the Geshekter posts on this panel).
Anderson, R. M., (1996): The spread of HIV and sexual mixing
patterns. In: AIDS in the World II, pp. 71, J. E. Mann & D.
J. M. Tarantola (eds.). Oxford Univ. press. Oxford.
Bregman, D. J. & A. D. Langmuir, (1990): Farr's law applied
to AIDS projections. J. Am. Med. Assoc. 263: 50-57.
Centers for Disease Control, (1999): U.S. HIV and AIDS cases
reported through June 1999. HIV AIDS Surveillance Report 11:
Duesberg, P. H., (1992): AIDS acquired by drug consumption
and other noncontagious risk factors. Pharmacology & Therapeutics
Duesberg, P. H., (1996): Inventing the AIDS Virus. Regnery
Publishing Inc., Washington.
Duesberg, P. H. & H. Bialy, (1996): Duesberg and the right
of reply according to Maddox-Nature. In: AIDS: virus- or drug
induced?, 5, pp. 111-125, P. H. Duesberg (eds.). Kluwer Academic
Duesberg, P. H. & D. Rasnick, (1998): The AIDS dilemma: drug
diseases blamed on a passenger virus. Genetica 104: 85-132.
Duesberg, P. H. & J. R. Schwartz, (1992): Latent viruses and
mutated oncogenes: no evidence for pathogenicity. Prog Nucleic
Acid Res Mol Biol 43: 135-204.
Fenner, F., B. R. McAuslan, C. A. Mims, J. Sambrook & D. O.
White, (1974): The Biology of Animal Viruses. Academic Press,
Inc., New York.
Fiala, C., 1998. AIDS in Africa: dirty tricks. New African,
Greenlee, R. T., T. Murray, S. Boldon & P. A. Wingo, (2000):
Cancer Statistics, 2000. CA cancer J Clin 50: 7-33.
Haverkos, H. W. & J. A. Dougherty (eds), 1988. Health Hazards
of Nitrite Inhalants. 83, US. Dept. Health & Human Services,
Konotey-Ahulu, F. I. D., (1987): Clinical epidemiology, not
seroepidemiology, is the answer to Africa's AIDS problem.
BMJ 294: 1593-1594.
Mullis, K., (1996): Foreword. In: Inventing the AIDS Virus,
pp. XI-XIV, P. Duesberg (eds.). Regnery Publishing, Inc. Washington
Mullis, K., (1998): Dancing naked in the mind field. Pantheon
Books, New York.
Seligmann, M., L. Chess, J. L. Faheyet al., (1984): AIDS-an
immunologic reevaluation. N. Engl. J. Med. 311: 1286-1292.
Widy-Wirski, R., S. Berkley, R. Downing, S. Okware, U. Recine,
R. Mugerwas, A. Lwegaba & S. Sempala, (1988): Evaluation of
the WHO clinical case definition for AIDS in Uganda. JAMA
260: (22) 3286-3289.