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Eleni Papadopulos-Eleopulos,
Department of Medical Physics, Royal Perth Hospital, Western Australia, 6001,
Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala

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In his Rapid Response “Request for the Perth Group”, 9 November, Peter Flegg wrote:

“The Perth Group has often asked questions in this debate of those who believe in the orthodox view that HIV exists. I try to answer queries whenever these concern a specific claim made by myself (but am not in the habit of trying to answer general questions that have been debated and explained ad nauseam by others)”.

This is not the case. For example, 9 of the questions we put to Peter Flegg in our penultimate response “PCP and “HIV””, 5 November remain unanswered. Neither has he told us what method he uses to diagnose PCP in his patients. Most importantly, once again Peter Flegg has failed to provide evidence that the “HIV” antibody tests are specific. The other questions Peter Flegg has not answered include the following:

1. Is Montagnier the discoverer of “HIV”?

2. What is the evidence that “HIV” exists?

3. What would he tell a mother of a child whose antibody test is positive at 18 months and why?

4. Is the immunosuppression induced by “HIV” the cause of KS?

5. Is KS an infectious disease?

6. Is KS sexually transmitted?

Peter Flegg wrote “However I would be grateful to the Perth Group for an explanation about one of their very specific statements. This concerned the 10 references cited to support their claim that human CD4 lymphocytes decline to less than 50/mm-3 in the absence of HIV infection (Sept 17th). Others and myself have pointed out that not one of the 10 papers cited supported this claim”.

In our Rapid Response “Causes of low CD4 counts” 14 September we wrote “In his rapid response "CD3 CD4 and all the more modern names", 3 September 2004, Nicholas Bennett wrote: "One has to ask just how the person got a CD4 count of less than 50 per microliter prior to HAART, the normal range being at the lowest ten times greater!" A person can get CD4 counts of less than 50 per microliter and immune suppression by repeated exposure to: drugs,1 2 semen, 3-6 Factor 8,7-9 and malnutrition.10”.

Our references 1-10 contain evidence that drugs (recreational), semen, factor VIII and malnutrition are immunosuppressive including a decrease in T4 cells. In his Rapid Response “Re: Causes of low Cd4 counts in AIDS-a question to the Perth Group”, 14 September Peter Flegg wrote “I was interested to read the Perth Group's assertion that "A person can get CD4 counts of less than 50 per microliter and immune suppression by repeated exposure to: drugs,(1 2) semen, (3-6) Factor 8,(7-9) and malnutrition.(10)" (Sept 14). I would also be fascinated to know how many of these articles actually do say the persons in question get CD4 counts of less than 50/mcl, and if they do in what percentage it has occurred. Would the Perth Group be so kind as to oblige by accurately quoting the relevant sentence from each of the studies in question? I only ask because I have no immediate access to the relevant articles in full text version, only in abstract form. Unfortunately in these I can find little to indicate that CD4 lymphopenia occurs to the profoundly low level of under 50/mcl in anybody”. Responding (“More on CD4s”, 30 September) we wrote “The fact is that there is nothing magic about 50 CD4 counts per microliter. Counts of less than 50 per microliter can be found in HIV negative patients…If something decreases the CD4 counts to "less than 300/mcl", there is no reason why it should not decrease them to 50 per microliter. As a physician, Peter Flegg is fully aware that if a drug, X, causes an effect, Y, then the magnitude of Y will depend on the dose, the frequency and the duration to which the patient is exposed to X”.

Answering (“Re: More on CD4s, 30 September), Peter Flegg wrote “They do now give references showing instances where low CD4 counts (<300/microlitre) have occurred in the absence of HIV, and then tag on the suggestion that: “If something decreases the CD4 counts to "less than 300/mcl", there is no reason why it should not decrease then to 50 per microliter.” Hmmm… how often would that happen, I wonder? Since I am a physician, I am also meant to know that “if a drug, X, causes an effect, Y, then the magnitude of Y will depend on the dose, the frequency and the duration to which the patient is exposed to X.” Well as a physician, I can say very few things in my experience of the human physiological response operates in such a simple, dose-dependent, linear manner, and there are clear limits for most parameters. (If a diuretic can make my serum sodium drop from 130mmol/l to 115mmol/l, will twice the dose make it drop to 100mmol/l, and four times the dose drop it to 70mmol/l?). I am however pleased to have been afforded this insight to the reasoning processes of the Perth Group, as it helps me understand some of their other deductions and conclusions”.

In our Rapid Response “”HIV”, Factor VIII and CD4s”, 14 October we wrote “We have never claimed that there is a linear relationship between the dose and the effect of drugs. If an agent decreases the CD4 counts to "less than 300/mcl, there is no reason why it should not decrease them to 50 per microliter", even if the "human physiological response" does not operate in "a simple, dose-dependent, linear manner"”.

In our Rapid Response “More on CD4s”, 30 September we put the question “…would Peter Flegg please let us know what he tells his haemophiliac patients is the cause for their decreased T4 cell counts?” Responding (“Re: More on CD4s”, 30 September) Peter Flegg wrote “I do not have any haemophiliac patients with HIV infection, but if I did, I would certainly tell any with CD4 count below 50/mcl that HIV was the cause”.

Does this mean that “HIV” is the only cause of a CD4 count is below 50/uL but not the only cause of a CD4 count above 50/uL?

Does it also mean that if an HIV antibody positive haemophiliac or drug user comes to Peter Flegg and is found have, for example, to have a CD4 count of 200/uL, he tells him the cause is factor VIII or IV drugs? If the same patient is exposed to UV radiation for a week and returns with a CD4 that has dropped to 50/uL he tells him that the cause is “HIV”? If a patient has PCP and a CD4 count of 200/uL the cause of PCP is factor VIII or IV drugs but if the CD4s are 50/uL the cause is “HIV”?

We asked Peter Flegg to read our paper “A critical analysis of the HIV-T4-cell AIDS hypothesis” and to make a point by point criticism. He had not done so. Why? In this paper he would read “A recent study of IV drug users in New York (Des Jarlais et al., 1993) showed that "The relative risk for seroconversion among subjects with one or more CD4 count <500 cells/uL compared with HIV-negative subjects with all counts >500 cells/uL was 4.53". A similar study in Italy (Nicolosi et al., 1990) showed that "low number of T4 cells was the highest risk factor for HIV infection", that is, decrease in T4 cells is a risk factor for seroconversion and not vice versa”.

In ““HIV”, Factor VIII and CD4s” 14 October we stated “In our paper "Factor VIII, HIV and AIDS in haemophiliacs: an analysis of their relationship" [1] we wrote: "It is generally accepted that in patients with haemophilia, HIV destroys T4 lymphocytes leading to acquired immune deficiency. Although this view has prevailed for ten years, at least one well known group of researchers of AIDS in haemophiliacs, that from the University of Bonn, questioned the above relationship between HIV and T4 cells as recently as 1990. "It is not clear whether the virus-host interrelationship in HIV infections is regulated primarily by the virus or by the host; i.e., are CD4+ cells depleted by non-viral mechanisms and does the virus adjust itself to the weakened defence? Or is the depletion of CD+ cells the consequence of the spread and cytopathogenicity of virulent viral variants, which developed at random from avirulent precursors?" (Schneweis et al., 1990). Discussing their data a year earlier they concluded "The results suggest that reactivation of HIV occurs when immune deficiency has become manifest" (Schneweis et al, 1989)…Numerous reports from many well known researchers of AIDS in haemophiliacs have shown that T4 cell depletion precedes "HIV infection".

1. Mortimer and his colleagues state, "The OKT4 subset was reduced in both seropositive (p < 0.01) and seronegative (p < 0.05) haemophiliacs but there was no difference between seropositive and seronegative patients" (Moffat, Bloom & Mortimer, 1985);

2. Weiss and colleagues report, "We have thus been able to compare lymphocyte subset data before and after infection with HTLV-III. It is commonly assumed that the reduction in T-helper-cell numbers is a result of the HTLV-III virus being tropic for T-helper-cells. Our finding in this study that T-helper-cell numbers and the helper/suppressor ratio did not change after infection supports our previous conclusion that the abnormal T-lymphocyte subsets are a result of the intravenous infusion of factor VIII concentrates per se, not HTLV-III infection" (Ludlam et al, 1985);

3. Kessler and colleagues found, "Repeated exposure to many blood products can be associated with development of T4/T8 abnormalities" including "significantly reduced mean T4/T8 ratio compared with age and sex-matched controls" (Kessler et al, 1983);

4. In 1984, Tsoukas et al observed that among a group of 33 asymptomatic haemophiliacs receiving factor VIII concentrates, 66% were immunodeficient "but only half were seropositive for HTLV-III", while "anti-HTLV-III antibodies were also found in the asymptomatic subjects with normal immune function". They summarised their findings as follows: "These data suggest that another factor (or factors) instead of, or in addition to, exposure to HTLV-III is required for the development of immune dysfunction is haemophiliacs" (Tsoukas et al, 1984); 5. By 1986 researchers from the CDC concluded: "Haemophiliacs with immune abnormalities may not necessarily be infected with HTLV-III/LAV, since the factor concentrate itself may be immunosuppressive even when produced from a population of donors not at risk for AIDS" (Jason et al, 1986);

6. In 1985 Montagnier (Montagnier, 1985) wrote: "This [clinical AID] syndrome occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV infection".”

Peter Flegg did not respond.

In our Rapid Response “More on CD4s”, 30 September we wrote “Lately, in a few of our rapid responses including the 14 September, we have drawn the attention to the fact, which Peter Flegg chose to ignore, that the "discoverers" of "HIV" themselves have shown that "HIV" is not sufficient or necessary for the decrease in T4 cells either in vitro or in vivo. Once again, in their experiments they have shown that:

(1) "HIV" + stimulation = decrease in T4 cells.

(2) Stimulation by itself = decrease in T4 cells.

(3) HIV" by itself = no effect.4 5"

Peter Flegg either:

(1) Disagrees with Gallo's and Montagnier's experimental findings, in which case he must tell them, and thus us, what is wrong with them; or

(2) Agrees with Gallo's and Montagnier's findings, in which case he, like us, comes up with an alternative reason for the T4 cell decrease in AIDS patients”. Again, Peter Flegg did not respond. Let us repeat: As a scientist and treating physician Peter Flegg must:

1. Either: (a) agree with some of the best known researchers of “HIV”/AIDS that in haemophiliacs and IV drug users, drugs and factor VIII are the cause of immunsuppression; or (b) present evidence that “HIV” and not the drugs, including clotting factor preparations, is the cause of the decrease in T4 cells;

2. Either: (a) agree with Gallo’s and Montagnier’s findings or (b) disagree with Gallo and Montagnier in which case he must tell them, and thus us and the readers of the BMJ Rapid Responses, what is wrong with their experimental findings, and provide evidence that “HIV” decreases the CD4 cells.

Unless Peter Flegg responds to 1 and 2 there can be no further scientific debate.

Competing interests: None declared