VIRUSMYTH HOMEPAGE


PERTH GROUP RESPONDS TO RASNICK

15 March 2000


Dear David,

We read with interest your detailed responses to the South African Health Ministry. We have seen fit to comment on some of them and thus avoid any generalisation that may be misinterpreted by a non-expert audience. We have itemised our answers in the same order as yours.

Kind regards,

Eleni Papadopulos-Eleopulos, Val Turner, John Papadimitriou, Helman Alphonso, David Causer, Barry Page.

Question 1: "What means and methods are used in the Public Health system to test the "HIV status" of individuals?"

Answer: "Our first reaction to this question is that the HIV antibody tests do not measure HIV at all. Neither does the Western blot (WB) test. These tests also do not test for AIDS".

Comment: Your answer implies that there are two types of tests, antibody tests and the Western blot, which is not the case. The Western blot (WB) is also an antibody test. Nobody has ever claimed that the antibody tests measure HIV or that they test for AIDS. According to all "HIV" experts, all the antibody tests, including the WB, detect antibodies to the "HIV proteins". They also claim that the tests are "HIV" specific, that is, they prove infection with HIV. If by "do not measure HIV at all" you mean the antibody tests are not at all specific to "HIV", then: (i) you are contradicting yourself. In answer to question 7 you state: "problems of cross-contamination [do you mean cross-reactivity?], poor levels of specificity and sensitivity, the fact that any of more than 70 diseases can give rise to a false positive test", imply the existence of HIV antibody tests. They may not be perfect but nonetheless at least sometimes they prove past or present HIV infection; (ii) given that the only proof that AIDS patients are infected with HIV is a positive antibody test, you would have to accept then that no proof exists that AIDS patients are infected with "HIV".

Your question: "A question we would ask the Health Minister is what evidence is there that people with antibodies to HIV live shorter, poorer lives than people in the same community who do not have antibodies to HIV? We know of no such evidence.

Comment: There is ample evidence showing a correlation, imperfect as it may be, between high levels of antibodies and "shorter, poorer lives". In fact, one does not need to search the scientific literature to realise that this is the case. For example, blood donors have low levels of antibodies in general and the rate of positive "HIV" antibody tests is commensurately low in this group of individuals. You accept that the rate of a positive antibody test is higher in individuals suffering from about 70 diseases, which include malaria and TB. Since there is a correlation between disease and a positive "HIV" antibody test, (whatever this may mean), it follows there must be a correlation between antibodies and "shorter, poorer lives".

Let us take a few more examples. There is evidence which shows that drug users have high levels of antibodies including autoantibodies, whose levels will obviously correlate with the quantity of drugs consumed.(1) According to the well known HIV expert, Myron Essex,(2) from Harvard University, autoantibodies give false positive "HIV" tests. As far back as 1986 another "HIV" expert, Harold Jaffe from the Centres for Disease Control, could not exclude the possibility that a positive "HIV" antibody test in all drug users may "represent false positive or non-specific reactions".(3) Obviously the higher the level of drugs consumed the higher the probability of "shorter, poorer lives". Since a correlation exists between the quantity of drugs consumed and the detection of a positive antibody test, (whatever its genesis), and the development of disease on the other, it follows then that a correlation will exist between antibodies and "shorter, poorer lives". Conversely, drug addicts who curtail their addiction, lose their "HIV" antibodies and live "longer, better lives".(4)

"According to Philip Mortimer, director of the Virus Reference Laboratory of the Public Health Laboratory Service, London, United Kingdom: "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".(5) Haemophiliacs are constantly exposed to "an array of alloantigens (and infectious agents)"(6) either via factor VIII or blood transfusion. This leads to hypergammaglobulinaemia and hypergammaglobulinaemia correlates with "HIV" seropositivity.(7) Haemophiliacs are known to have high levels of anti-lymphocyte antibodies, 74% have anti-cardiolipin antibodies, 28% anti-nuclear antibodies and 85% immune complexes.(8) HIV researchers accept that "antilymphocyte, antinuclear and other autoantibodies" gave rise to false positive "HIV" antibody tests.2, (9) It goes without saying that the frequency and quantity of blood and factor VIII administered correlates with the severity of haemophilia, that is, with "shorter, poorer lives".

The introduction of factor VIII led to a dramatic decrease in haemophilia deaths from bleeding but it also had some harmful effects including myocardial ischaemia, visual disturbances, headache, dyspnoea, bronchospasm, hypotension and anaemia(10-12) Factor VIII preparations contain immunoglobulin which may produce systemic reactions such as pruritus, chills, fever, tremor, flushing, malaise, nausea, vomiting, back pain.(13)

In 1985 Robin Weiss and his colleagues concluded: "the abnormal T lymphocyte subsets [decrease in T4 cells AIDS] are a result of the intravenous infusion of factor VIII concentrates.(14) One year later, researchers from the CDC wrote: "the factor [VIII] concentrate itself may be immunosuppresive even when produced from a population of donors not at risk for AIDS".(15) It is also of interest to note that in 1985, before HIV was generally accepted as being the cause of AIDS, Montagnier wrote: "This syndrome [clinical AIDS] occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV infection".(16) Obviously the clinical symptoms and diseases as well as the decrease in T4 lymphocytes induced by antigenic stimulation with factor VIII and blood transfusions will correlate with the quantity and the frequency of their administration.

Since a correlation exists between the quantity of factor VIII and blood administered to the haemophiliacs and the development of a positive antibody test (whatever it means) and disease, it follows that a correlation will exist between antibodies and "shorter, poorer lives".

Individuals with AIDS, AIDS-related complex and those at risk, have circulating immune complexes, rheumatoid factor, anti-cardiolipin, anti-nuclear factor, anti-cellular, anti-platelet, anti-red cell, anti-actin, anti-DNA, anti-tubulin, anti-thyroglobulin, anti-albumin, anti-myosin, anti-trinitrophenyl and anti-thymosin antibodies.(17, 18) Anti-lymphocyte auto-antibodies have been found in 87% of HIV+ patients, and their levels correlate with clinical status.(19, 20) Many of these are autoantibodies and the higher the affinity and the higher the titre, the higher the probability of a tissue damaging autoimmune inflammatory response and eventual organ failure. The autoantibodies precede and predict tissue damage and organ failure. In the case of some diseases such as autoimmune thyroid disease and insulin dependent diabetes mellitus, such antibodies are detectable for many years or even decades before overt disease ensues and causes "shorter, poorer lives".

The notion that a non-specific laboratory test reliably predicts disease is nothing new and is quite familiar and useful to clinicians. For example, it is difficult to imagine anything less specific than the erythrocyte sedimentation rate (ESR-the speed at which a vertical column of red blood cells gravitates downwards in a test tube). Yet if the ESR is elevated, this "must always be taken to indicate disease if anaemia and pregnancy are excluded".(21) Similarly, although there is no proof that the antibodies which react with the "HIV" proteins are directed against a retrovirus, nonetheless the evidence shows that such antibodies, at least in the risk groups, predict a propensity to particular diseases defined as "AIDS".(22-24)

Your question: "Furthermore, why are antibodies to HIV a sign of impending disease and death? Antibodies are a sign of immunity, not imminent death? We know of no answer to this question".

Comment: The answer is simple: the antibodies may not be a sign of immunity. Your question seems to paraphrase one of Peter's main arguments against the HIV theory of AIDS. He claims that after antibody to viruses, including HIV, appear in the blood, they neutralise the virus and since AIDS develops after the appearance of antibodies, HIV cannot be the cause AIDS. However, as Weiss and Jaffe point out: "Most persistent infections, however, proceed in the presence of a humoral [antibody] response".(25) It is the individuals who have persistent antibodies to Treponema pallidum who develop secondary syphilis, not those who are negative. Not only are the antibodies not a sign of immunity but in some cases, such as Dengue fever, the viral antibodies exacerbate the disease.(26) As far back as 1935, Albert Sabin, in a series of experiments designed to investigate the "mechanism of immunity to filterable viruses" (retroviruses and thus "HIV" by definition are filterable viruses) concluded that: "The results with the cultures containing the "treated" virus are not only an additional control for the above experiments, but also a confirmation in vitro of the observations made in vivo in the preceding investigation, and show quite definitely that the immune serum does not alter the physical state of the virus in a way which would render it non-infectious…For even among the ordinary bacteria, the anti-bacterial antibodies are not always the ones that protect against infection...It was, therefore, difficult to escape the conclusion that even in the presence of tissue, the action of the protective substance was not upon the virus, but rather upon the tissue. This effect upon the tissue was such that it became refractory to infection and unsuitable for the multiplication of virus. That this refractory state does not represent a permanent, irreversible change in the cells is evident from the observation that by profuse washing it was possible to render the tissue susceptible again".(27-30)

In a paper entitled "Delineation of putative mechanisms involved in antibody-mediated clearance of rabies virus from central nervous system" the authors concluded that: "The protective activity of a particular mAb [monoclonal antibody] in vivo did not correlate with its virus-neutralizing activity in vitro…these mAbs block virus infection by an inhibition of the intraendosomal acid-catalysed fusion step that leads to virus uncoating" and thus to RNA transcription and virus multiplication.(31) Depending on the initial conditions of the terrain and the dose/nature of the antibody, the change induced by the antibodies may not affect the disease (and virus multiplication), induce immunity or may lead to exacerbation of the disease.

Question 2: "What definition is used, again in the Public Health system, to classify a person as being afflicted with AIDS"?

Answer: In your answer you state that "Childhood AIDS is AIDS by association. A child can be labelled with AIDS because the mother has antibodies to HIV".

Comment: In no country or continent, including Africa, is a child said to have AIDS because the "mother has antibodies to HIV". According to the Bangui definition of AIDS in African children: "Paediatric AIDS is suspected in an infant or child presenting with at least 2 of the following major signs associated with at least 2 of the following minor signs in the absence of known cases of immunosuppression such as cancer or severe malnutrition or other recognised etiologies.

1. Major signs

  1. weight loss or abnormality slow growth;
  2. chronic diarrhoea > 1 month;
  3. prolonged fever > 1 month.

2. Minor signs

  1. generalised lymphadenopathy;
  2. oro-pharyngeal candidiasis;
  3. repeated common infections (otitis, pharyngitis, etc);
  4. persistent cough;
  5. generalised dermatitis;
  6. confirmed maternal LAV/HTLV-III infection".32

Question 3: "Of the people determined to have died of AIDS, what "opportunistic disease" was identified as having been the immediate cause of death?"

Answer: "Mr President, we would like to know how doctors know the difference between:

  1. pneumonia and AIDS pneumonia?
  2. tuberculosis and AIDS tuberculosis?
  3. intractable diarrhoea and AIDS intractable diarrhoea?
  4. meningitis and AIDS meningitis?
  5. generalised septicemia and AIDS generalised septicemia?
  6. wasting syndrome and AIDS wasting syndrome?
  7. Kaposi's sarcoma and AIDS Kaposi's sarcoma?
  8. cardiomyopathy and AIDS cardiomyopathy?
  9. multi-system failure and AIDS multi-system failure?

Comment: One does not answer a question with a series of questions. If you wish to use this type of reasoning then you should ask a much more fundamental and relevant (as far as the HIV hypothesis of AIDS is concerned) question. Namely, how do doctors know the difference between a true and a false positive HIV test in the individuals with the diseases you list, when for example it is accepted by even well known HIV experts that at least 50% of AIDS patients with mycobacterial diseases (such as TB) and their contacts have false positive HIV antibody tests which would satisfy even the most stringent criteria for a positive test?(2)

Question 5: "Has any research been done on the health profiles on the population where allegedly it has been found that there are large numbers of "HIV positive people" (e.g. In KZN)?".

Answer: In your answer you state "We know of no study that shows that AIDS is sexually transmitted".

Comment: It is true that at present no study exists which proves that AIDS is a bidirectionally sexually transmitted disease. However, it is equally as true, as we repeatedly stressed to Charles during his visit late last year, that at present there is ample theoretical, experimental and epidemiological evidence which shows that AIDS and a positive "HIV" antibody can be sexually acquired. We also have pointed out that if one has problems understanding the theoretical evidence or, for one or another reason, cannot read all the experimental and epidemiological data, then suffice to read the numerous publications from:

1. The Multicenter AIDS Cohort study the largest, longest, best designed and executed prospective study in gay men.(33-38)
2. Nancy Padian's study, the longest, largest study in heterosexuals.(22, 39-42)

to realise that:

(a) AIDS and a positive "HIV" test can be sexually acquired.
(b) 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.
(c) 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.
(d) 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"(43) which is important. In other words, 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 sexual intercourse, for AIDS to appear a very high frequency of receptive anal intercourse over a long period is necessary. AIDS is more like anal (Daling, 1987 #1346; Kondlapoodi, 1982 #1348) and cervical cancer.(Reid, 1978 #1347 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 the development of AIDS.

There are several reasons why, unlike sexually acquired anal and cervical cancer, AIDS became a separate disease. They include the following:

(i) The very high level of sexual activity in a very small fraction of gay men. In 1989, Jad Adams, a medical journalist wrote: "Looking at homosexual men with and without the disease it looked clear that the AIDS patients were mainly those who had a large number of sexual contacts (and 'large' often means twenty a week); those who were receptive to anal intercourse and those who practised… brachioproctal intercourse...For just over a decade it was possible for anyone, waiters and diplomats and building workers, to enjoy orgies every night".

In an interview Camille Paglia gave to Huw Christie in 1996 she stated that in the 1960's and 1970's "gay men were pushing the limits of the human body throughout that period…I have constantly said of the gay men of my generation that they challenged Nature and lost. But I'm saying that is noble and worthy. It's like the great Romantics".(44).

(ii) The same minority of gay men who practised passive anal intercourse in high frequency were also exposed to drugs, including nitrites. These drugs acting either alone or in synergism with passive anal intercourse, may also have contributed to the appearance of AIDS;(45-48)

(iii) While anal and cervical cancer acquired through sexual activity are dispersed through the world, the small minority of highly sexually active gay men are localised in a small number of cities making it easier for physicians to see the relationship between sexual activity and AIDS.

To claim that sexual activity, either alone or in combination with drugs, plays no role in the acquisition of AIDS, especially in gay men, is not only scientifically incorrect but, from a public health point of view, dangerous.

Question 6: "Has any research been done on 'HIV positive' infants, children and orphans with regard to their health profiles, those of their mothers and families, as well as the lifestyles and socio-economic circumstances of the mothers and families?"

Answer: We would have phrased the question this way: Has any research shown that HIV positive infants, children and orphans live shorter or poorer quality lives as compares to HIV negative infants, children and orphans in the same community? In other words, do antibodies to HIV matter at all? To the best of my knowledge, this question has neither been asked nor answered in the mainstream scientific and medical literature.

Comment: Children with "malaria, tuberculosis or malnutrition" in communities where they are present in high frequency will have "shorter and poorer quality lives" compared to the healthy and well nourished children in the same community. It is also a fact that malnutrition (weight loss), malaria and TB are associated with a higher rate of positive "HIV" antibody tests.(2, 49-51) Since a correlation exists between a disease and shorter poorer lives and also between disease and a positive antibody test; it follows that a correlation exists between a positive antibody test and "shorter and poorer lives".

Question 7: "On what do we base statistics we publish occasionally on the incidence of HIV and AIDS, and how do we arrive at the projection?"

Answer: In your answer you state: "Since 1994, tuberculosis itself has been considered an AIDS-indicating disease".

Comment: Extrapulmonary TB has been considered an AIDS indicator disease since September 1987, and pulmonary TB since January 1993.

Maybe we should conclude by reminding ourselves of Plato's advice: "...we are not simply contending in order that my view or that of yours may prevail, but I presume we ought both of us to be fighting for the truth..."


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