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“The only thing necessary for these diseases to the triumph is for good people and governments to do nothing.”

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Does it prove that HIV causes AIDS?

By Vladimir Koliadin

August 1998

In a British-funded study, it was found that mortality in young (13-44) adults in Uganda is 60 times higher for HIV-seropositives than for seronegatives. Mainstream AIDS scientist present these results as a strong evidence that HIV is the cause of AIDS. Such arguments are very persuasive to public and most scientists, even though being essentially flawed. Elementary analysis shows the results don't confirm, but refute the official HIV-causes-AIDS hypothesis, and they are in good agreement with predictions of the alternative hypotheses advanced by "AIDS-dissidents".

1. Introduction

It is a frequent situation in natural sciences when the same facts may be explained by several competing hypotheses. Moreover, some facts may seem irrefutable evidence for a hypothesis at first sight, but, after closer examination, occur an evidence of the reverse. As far as scientific community and public normally have some preconceived ideas (e.g. that HIV causes AIDS), both easily accept such pseudo-evidences, and fail to notice the obvious logical flaws. The stronger the collective belief in some idea, the smaller the chance that the flaws in the "evidence" will be noticed. Such situation makes it easy for wrong ideas to be widely accepted as the ultimate truth, seemingly supported by a huge body of incontrovertible evidence. In this paper, I am going to illustrate this general point by an example from AIDS research. Results of a study conducted in Uganda [1] are often referred to by mainstream AIDS scientists as a strong evidence of the causal role of HIV in AIDS. Even though this seems to be undoubtedly true at first sight, in reality, the results are in serious contradiction with predictions of the official HIV-causes-AIDS hypothesis, and confirm the alternative hypotheses which assume that HIV is not a causal factor of AIDS. Unfortunately, the obvious logical flaws in the "evidence" remained unnoticed by both mainstream AIDS scientists and their opponents (at least I am not aware about any publication which would have spotted the logical errors in the seeming "evidence").

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2. Some facts about mortality and seroprevalence in Uganda

Results of the study under investigation were described in [1]. Below, I cite from [2] only a concise summary:

"In this study, a rural population [in Uganda] of about 10,000 was screened for HIV infection using highly specific tests. The seroprevalence of HIV infection in those aged 13-44 was 9.6%. During follow up over two years, eight deaths were obserevd in 5,800 man-years among seronegatives in this age-group (1.4/1000 m-y), compared to 51 deaths in 534 man-years among the seropositives (96/1000 m-y). The age adjusted rate ratio was 60 ...".

Thus, mortality was more than 60 times higher among HIV-seropositives at age 13-44 than among their HIV-negative counterparts. To interpret these results, it is worth saying a few words about alternative hypotheses on nature of HIV-seropositivity and to compare predictions of these hypotheses to that of the official HIV-causes-AIDS theory.

3. Alternative hypotheses on nature of HIV-seropositivity

There are several hypotheses which explain the observed correlation between HIV-seropositivity (a positive test for "HIV-antibodies") and severe opportunistic AIDS-defining diseases. In spite of essential distinctions, all the alternative hypotheses bear a common feature - HIV-seropositivity is regarded as a consequence (marker) of low health status and diseases, not as the cause.

First two hypotheses hold that HIV-seropositivity is actually a consequence of HIV-infection, but HIV is a benign retrovirus. In contrast to the official HIV-causes-AIDS hypothesis, the two hypotheses regard HIV-infection as a factor concomitant with diseases, but not their cause. Hypothesis I: Correlation between HIV and AIDS is because HIV is only a marker of specific unhealthy lifestyle typical to some segments of population - promiscuous gays, drug users, etc. [3]. Hypothesis II: HIV is a harmless ubiquitous retrovirus which is capable to replicate only if health is already compromised. Thus, HIV-infection is a mild opportunistic infection - an early indicator of some problems with immunity.

Other two hypotheses hold that HIV does not exist at all as an exogenous transmissible agent. The laboratory phenomena observed in cell cultures and interpreted by the mainstream science as evidence of presence of HIV are explained by mechanism which have nothing to do with a virus.

Hypothesis III: The "HIV-proteins" do not belong to a virus, but are of intracellular (endogenous) nature [4,5]. The genes which encode the structure of these proteins are normally silent constituents of the human genome (most of human genes are normally silent - that is, the proteins they encode are not normally produced) [6]. Only under certain abnormal conditions, e.g. in course of catabolic stress, the genes are switched on and the cells start to produce these proteins. As far as the proteins are foreign for the immune system, specific antibodies are produced against them. These antibodies are detected by the HIV-antibody tests, and corresponding messenger RNA are detected by the "viral load tests".

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Hypothesis IV: The antibodies to which the HIV-antibody tests react are not specific at all - they belong to non-specific immunoglobulins. Under certain conditions (e.g. overstimulation by foreign antigens, catabolic stress), B-cells become hyperactive and produce immunoglobulins with higher non-specific affinity than usually [6]. Both ELISA and Western Blot tests are abnormally sensitive to non-specific binding because both are based on "sandwich" principle [7]. Hence, a positive HIV-antibody test is only a marker indicating that B-cells are hyperactive (which is a hallmark of AIDS and many other abnormal states of organism).

Thus, there is no shortage of alternative explanations of the HIV-seropositivity and its association with severe diseases. Comparative analysis of the alternative hypothesis lies beyond the scope of this paper. The only thing which will be taken into account here is that all the alternative hypotheses regard HIV-seropositivity as a marker of compromised health or other disease-causing factors. Therefore, I will refer to all these hypotheses as "marker hypotheses", for short.

4. Predictions of the competing hypotheses

If HIV-seropositivity is only marker of deteriorated health and diseases, HIV-seropositive individuals will show significantly higher morbidity and mortality than HIV-seronegative ones. The official HIV-causes AIDS hypothesis also predicts higher mortality in the HIV-seropositive group. Hence, the fact that mortality is much higher in seropositives than in seronegatives is explainable by the official as well as by the alternative hypotheses, and it cannot be an evidence that HIV causes AIDS. Is it possible to discriminate between the official and the alternative "marker hypotheses"? If to focus only at mortality in HIV-seropositive group, it is hardly possible - all the hypotheses predict that mortality and morbidity among HIV-seropositives will be higher than among HIV-seronegatives. But it seems to have remained unnoticed by both mainstream AIDS scientists and their opponents that analysis of mortality in HIV-negatives can provide important clues [7]. If HIV is actually a new pathogen and causes additional mortality independently on other causes of death typical to this region (as the official theory holds), mortality in HIV-negative population should be about the same as before HIV-epidemic. Prediction of the "marker hypotheses" is radically different - mortality in seronegatives has to be lower than the death rate usual to this population. Actually, let HIV-seropositivity is only an indicator of diseases and compromised health. Then, a great proportion of the individuals who were to have died from causes usual to this region and not related to HIV (mainly various infectious and parsitic diseases) will fall into the HIV-seropositive group. Therefore, the total number of deaths in the HIV-seronegative group will be lower than that expected from usual rates of non-HIV-related mortality.

5. Comparing predictions of the competing hypotheses to reality

Mortality in HIV-negative group in the investigated population of Uganda was 1.38 per 1000 person-years (8 deaths in 5800 person-years of observation). Is it reasonable to assume that this mortality rate is usual for a rural area of Uganda? (The terms "usual mortality" or "usual deaths" means here the deaths not related to HIV and expected from the death rates observed earlier than the hypothetical HIV-epidemic began). Because any more or less reliable statistical information is absent about the usual mortality in Uganda, we will use indirect approach to answer this question.

It is well known that usual mortality among young adults in many African countries, including Uganda, is much higher than that in developed countries - a great proportion of population die young, mainly from various parasitic and infectious diseases. This difference is explained by general poverty, malnutrition, lack of adequate medical service typical to many African countries. Is the annual mortality rate in 1.38/1000 observed in HIV-negative Ugandans compatible with this general information? The answer is definitely negative at least on two counts. First, rough calculations show that such annual mortality rate is equivalent to 96% survival in 30 years (only 4% die during 30 years, say from age 13 to 44). This is in obvious contradictions with the fact that a significant proportion of the population die young. Second, mortality rate in HIV-negative Ugandans at age 13-44 is even lower than mortality in the USA observed in the pre-AIDS era: in 1980, 157,685 deaths were registered in the USA at ages 15-44, and the population at this age was 105,203,377. This gives general mortality rate 1.5/1000 (higher than the 1.38/1000 in HIV-negative Ugandans). It is unreasonable to believe that usual mortality in a rural population of Uganda is about the same as in the USA - one of the most prosperous country all over the world. Hence, the observed mortality in HIV-seronegative population of Uganda is definitely much lower than the usual mortality rate typical to this population. In other words, most of the Ugandans who were to have died even without the hypothetical HIV epidemic, occurred to be HIV-seropositive when tested for "HIV-antibodies". This means that either HIV (if it really exists) "prefers" the individuals with compromised health and at high risk of diseases typical to this region, or that HIV-seropositivity is a biochemical marker of compromised health and these diseases.

6. Quantitative analysis

How much reality departs from predictions of the official HIV-causes-AIDS hypothesis? Let us make some quantitative estimates. We assume first that HIV is actually a new deadly pathogen and it infects individuals irrespective to their health status - that is the HIV-causes-AIDS theory is correct. In this case, the "usual" deaths (not related to HIV) will be distributed between HIV-positive and HIV-negative groups in the same proportion as the sizes of these groups, and mortality in the HIV-negative group would be equal to the "usual" mortality - because HIV-related deaths, even if they are real, would fall into the HIV-positive group. Let, for example, usual annual mortality is 3/1000 (that is about 2.2 times higher than mortality observed in HIV-seronegative Ugandans). The average expected number of "usual" deaths would be 1.6 (=534*0.003) in the HIV-positive group (534 person-years), and 17.4 (=5800*0.003) in the HIV-negative group (5800 person-years). Expected ratio is 0.092 (=1.6/17.4). The actual (observed) number of deaths in HIV-negative group is only 8. Hence, the remaining 9.4 (=17.4-8) deaths expected for "usual" mortality fell into the HIV-positive group, and the total number of "usual" deaths in this group is 11 (=1.6+9.4). Thus, the actual distribution of "usual" deaths between HIV-positive and HIV-negative groups is 11 against 8. The ratio of these numbers (1.375) is 15 times higher than that expected for HIV-causes-AIDS hypothesis (0.092). (It may seem strange at first sight that, if "usual" mortality is only 2.2 times higher than the observed mortality in the HIV-negative group, the ratio between observed and expected proportions is so high as 15. But it is a natural consequence of the fact that size of the HIV-positive group is more than 10 times smaller than the size of the HIV-negative one.)

As far as precise value for "usual" mortality in this region of Uganda is not known, computations were carried out for several values of the "usual" mortality. The results are summarized in the table. Column 2 shows probability of survival in 30 years - it helps to decide whether the "usual" mortality rate in column 1 is compatible with the qualitative information that a great proportion of population die young. The ratio between expected and actual proportions (computed as described above) is shown in column 3.

  "Usual" mortality   Survival in 30 years  Ratio of proportions
(1/1000 peson-years)      (percent)        (observed/expected)
      1.38                  95.9                 1.0
      3.0                   91.4                14.9
      5.0                   86.0                32.1
      7.0                   81.0                49.3
      9.3                   75.6                69.1

It is reasonable to assume that usual mortality rate in young adults in Uganda is at least several times higher than in the USA (1.5/1000). If the usual mortality in Uganda is, say 5/1000 person-years, the observed distribution of usual deaths between seropositive and seronegative groups differs 32 times from that expected for the HIV-causes-AIDS hypothesis (see table). There are also no any serious reasons to believe that the observed annual rate of overall mortality among HIV-negatives and HIV-positives combined (9.3/1000 person-years) differs from the usual death rate for this population. At least 75% survival in 30 years is quite compatible with the qualitative information that significant proportion of the local population die young. In this case, we might conclude that association between HIV-seropositivity and usual mortality is 69 times higher than that expected from the predictions of the HIV-causes-AIDS theory.

7. Can we trust the mainstream AIDS science?

The elementary analysis described above easily revealed strong inconsistencies between predictions of the official HIV-causes-AIDS theory and real facts, and showed that the facts are in good agreement with predictions of the alternative "marker hypotheses". Nevertheless, mainstream AIDS scientists ignore these obvious inconsistencies and present results of the study [1] as a strong evidence of the HIV-causes-AIDS theory. For some reasons, scientific community and public have proven to be incapable to analyze such pseudo-evidences more or less critically - they readily accepted them as true evidences of the official theory. This lack of critical thinking is a bad symptom - it is a sign that scientific enterprise lost its ability to judge facts objectively and independently on collective beliefs. This raises a more general question: To which extent the various experimental and observational "evidences" of the HIV-causes-AIDS theory published by mainstream AIDS scientists are true evidences? Critical and independent reevaluation of such "evidences" is urgently needed, at least as far as we wish to arrive at more or less objective picture of reality and to establish actual causes of AIDS and ways to treat and prevent this disease.


The observed death rate in HIV-seronegative Ugandans (1.38/1000 person years) is definitely lower than the usual (not related to HIV) death rate typical to this region. This is in perfect agreement with predictions of the alternative hypotheses which regard HIV-seropositivity as only a marker of deteriorated health and diseases usual to this region; and this contradicts to predictions of the official HIV-causes-AIDS theory. Quantitative estimates show that actual distribution of "usual" deaths between HIV-seropositive and seronegative population differs from that predicted by the HIV-causes-AIDS theory 30-70 times. Nevertheless, mainstream AIDS science presents the results as a strong evidence of the HIV-causes-AIDS theory, and the rest of scientific community and public gullibly accepts them as such.


1. Mulder, D.W., Nunn, A.J., Kamali, A. et al. Two-year HIV-1-associated mortality in a Ugandan rural population. Lancet v.343, pp. 1021-1023 (April 23, 1994)

2. Robinson, J. and Hayes, R. The other side. RSS News v.22, no 10, p.13 (1994)

3. Duesberg,P.H. AIDS acquired by drug consumption and other noncontagious risk factors. Pharmac.Ther. v.55, pp.201-277, 1992

4. Papadopulos-Eleopulos, E., Turner, V.F, Papadimitriou, J.M. Is a positive Western Blot proof of HIV infection? Bio/Technology v.11, pp.697-707, June 1993

5. Papadopulos-Eleopulos,E., Turner, V.F, Papadimitriou, J.M., Causer, D. The isolation of HIV: Has it really been achieved? The case against. Continuum (supplement) v.4, no.3, pp.1-24, September/October 1996

6. Koliadin, V.L. Critical analysis of the current views on the nature of AIDS. Genetica v.95, pp.71-90, January/March 1995

7. Koliadin, V.L. What causes a positive test for HIV antibodies. In "UN-Public Information Dossier, 2nd Edition" (IFAS - International Forum for Accessible Science), pp. 48-55, April 1998.