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Rapid Responses: Rapid Responses published:
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AIDS - HAART retroviral theraqpy revisited
- Etienne P. de Harven, Christian Fiala (14 March 2004)
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Re: AIDS - HAART retroviral theraqpy revisited
- Peter J Flegg (16 March 2004)
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Cause of beneficial effects of HAART potentially misinterpreted
- Nicholas D. Chester (2 April 2004)
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Re: Cause of beneficial effects of HAART potentially misinterpreted
- Peter Flegg (5 April 2004)
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HAART: One foot on the gas pedal, the other on the brake!
- David Rasnick (5 April 2004)
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Re: Cause of beneficial effects of HAART potentially misinterpreted
- Eleni Papadopulos-Eleopulos, Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala (6 April 2004)
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Perth Group misinterpretations
- Peter Flegg (9 April 2004)
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Can Peter Flegg prove 'HIV' existence?
- Alexander H Russell (9 April 2004)
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Response to Russell: even Duesberg has "proved HIV existence"
- Peter Flegg (15 April 2004)
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Response to Peter Flegg
- Alexander H Russell (21 April 2004)
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Response to Alex Russell
- Peter Flegg (22 April 2004)
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Flegg has still not proved the existence of 'HIV'
- Alexander H Russell (24 April 2004)
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Re: Flegg has still not proved the existence of 'HIV'
- Etienne de Harven (27 April 2004)
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The dissident Emperor's new clothes.
- Peter Flegg (27 April 2004)
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Reviving Flegg's fading hope
- Alexander H Russell (28 April 2004)
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HIV-induced apoptosis
- Peter Flegg (29 April 2004)
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Re: HIV-induced apoptosis-correction
- Peter Flegg (29 April 2004)
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Final challenge to Flegg
- Alexander H Russell (29 April 2004)
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Final response to Russell
- Peter Flegg (30 April 2004)
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Re: Perth Group misinterpretations
- Eleni Papadopulos-Eleopulos, Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala (30 April 2004)
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Dr. Flegg's continued obfuscation: where is the evidence that 'HIV' exists?
- Alexander H Russell (3 May 2004)
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Re: Response to Russell: even Duesberg has "proved HIV existence"
- Eleni Papadopulos-Eleopulos, Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala (3 May 2004)
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Re: Re: Response to Russell: even Duesberg has "proved HIV existence"
- Simon Portsmouth (3 May 2004)
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Re: Re: Response to Russell: even Duesberg has "proved HIV existence"
- Peter Flegg (4 May 2004)
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Re: Re: Re: Response to Russell: even Duesberg has "proved HIV existence"
- Eleni Papadopulos-Eleopulos, Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala (6 May 2004)
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Duesberg has not provided visual proof for the existence of 'HIV'.
- Alexander H Russell (10 May 2004)
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Re: Duesberg has not provided visual proof for the existence of 'HIV'.
- Peter Flegg (11 May 2004)
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Perth Group misinterpretations and HIV-apoptosis
- Peter Flegg (11 May 2004)
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Re: Re: Duesberg has not provided visual proof for the existence of 'HIV'.
- Alexander H Russell (25 May 2004)
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Re: Re: Re: Duesberg has not provided visual proof for the existence of 'HIV'.
- Peter J Flegg (26 May 2004)
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here we go again!
- Bob Bury (27 May 2004)
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Etienne P. de Harven, Emerit.prof. Univ of Toronto 06530 Saint Cézaire, France, Christian Fiala
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.AIDS – HAART Retroviral therapy revisited. There are reports about impressive clinical improvements, experienced by advanced AIDS patients shortly after receiving HAART or tri-therapy. These sometimes spectacular clinical benefits (occasionally referred to as the Lazarus effect), are universally interpreted as an unambiguous confirmation of the causal relationship between HIV and AIDS, simply because these drugs supposedly have antiretroviral properties. However, advanced AIDS patients most frequently suffer from severe opportunistic infections, frequently caused by the proliferation of Candida albicans (Trush) and/or of Pneumocytis carinii (PCP). This cannot be underemphasized, particularly because, in recent years, two groups of researchers have demonstrated and published (1, 2) experimental data clearly establishing that the anti-proteases (that are parts of the HAART protocol) are highly effective against both Candida and against Pneumocystis. These two papers did not apparently receive the attention they deserve, although both were published in the Journal of Infectious Diseases, in 1999 and in 2000. But how can we exclude that the significant clinical improvements observed, are the result from the antibiotic effects of the anti-proteases against Candida and against Pneumocystis since it is well known that these two microorganisms are, in a majority of cases, the culprits of grave opportunistic infections severely compromising the clinical course of advanced AIDS victims? This question deserves immediate attention, because if the hypothesis is correct, then the favorable effects of HAART do not contribute any additional evidence in support of the alleged link between HIV and AIDS, and the patients should rather be treated with antibiotics and anti-fungal drugs, which have less side effects than HAART. Etienne de Harven, MD Emerit. Prof. (Pathology), University of Toronto e-mail pitou.deharven@wanadoo.fr References; 1. Cassone A, De Bernardis F, Torosantucci A, Tacconelli E, Tumbarello M and Cauda R. In vitro and in Vivo anticandidal activity of human immunodeficiency virus protease inhibitors. Jour. Infect. Diseases 1999; 180:448-453. 2. Atzori C, Angela I, Mainini A, Agostini F, Micheli V, and Cargnel A. In Vitro activity of human immunodeficiency virus protease inhibitors against Pneumocystis carinii. Jour. Infect. Diseases 2000; 181:1629-1634. Competing interests: None declared |
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Peter J Flegg, Consultant Physician Blackpool Victoria Hospital, UK FY3 8NR
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I am glad Etienne de Harven acknowledges the often spectacular clinical benefits that occur in people on highly active antiretroviral therapy (HAART). I have become so used to HIV dissidents blaming the drugs for causing AIDS that it makes a nice change to see one of them attribute clinical recovery to their use (albeit for the wrong reasons, namely that protease inhibitors may exert an anti-Candidal and anti-Pneumocystis effect). However, he is grasping at straws if he thinks this could be used to deny the facts about HIV and its therapy. I would be fascinated to hear how his hypothesis explains the following: • Initial HAART regimens usually consist of drug combinations that specifically exclude protease inhibitors (but AIDS patients respond just as well to these non-protease regimens). • AIDS patients without Candida or Pneumocystis respond well to HAART (indeed these infections are only 2 of the many different conditions that constitute AIDS. Does De Harven propose HAART has specific effects against, say, Cytomegalovirus, JC virus or mycobacteria?). • Since the start of the AIDS epidemic there have been effective treatments for Candida and Pneumocystis, but it was not until the arrival of HAART that patients experienced miraculous “Lazarus effects” leading to sustained clinical and immunological recovery. (De Harven suggests that we merely treat patients with antibiotics and antifungals to avoid side effects of HAART, but as a clinician with over 20 years in the field, I can assure him that this alone is insufficient, and it is only the advent of suppressive retroviral therapy that has brought about this change). • Patients on protease-based HAART are still susceptible to Candida and Pneumocystis infection, and indeed some patients develop these infections despite being on HAART. The risk of developing these infections correlating directly with the extent of cell-mediated immunodeficiency, and not simply with which HIV drugs the patient is on. Protease inhibitors are patently ineffective therapeutic or prophylactic drugs for this purpose. • Treatment naïve patients presenting with infections such as Pneumocystis are never immediately commenced on HAART. Rather, the Pneumocystis is treated first with appropriate antimicrobials, and HAART is only commenced later, after the exclusion of other possible latent opportunistic infections such as atypical mycobacteria or CMV. It is clear that De Harven is not a clinician with experience in managing AIDS patients, or he would not propose such a convoluted hypothesis in the hope of disproving the link between HIV and AIDS. No doubt we will see further contrived attempts to explain away all these inconsistencies. The simplest explanation is usually the best (remember William of Occam and his principle of parsimony?) – namely that HIV causes immunodeficiency, and that HAART suppresses HIV and this results in immune recovery. It is also rather disingenuous of De Harven to use the citations he quotes to cast doubt on the link between HIV and AIDS. Yet again, as with most dissident claims, he only sees what he wishes to see in the studies in question. They do raise the possibility that protease inhibitors have a direct antimicrobial effect. In the first paper (1) this is thought to be by inhibition of a Candida-specific secretory aspartyl protease, and a therapeutic effect was seen within an experimental model. In the second study (2) Pneumocystis aspartyl protease “seemed to be affected” by protease inhibitors in vitro. Nowhere does this paper claim that HAART is “highly effective” against Pneumocystis as de Harven states. This study specifically acknowledges that the dramatic recent decline in opportunistic infections such as Pneumocystis is clearly and largely due to the induction of immune reconstitution by HAART; however this is something De Harven prefers not to mention. (1). Cassone A, De Bernardis F, Torosantucci A, Tacconelli E, Tumbarello M and Cauda R. In vitro and in Vivo anticandidal activity of human immunodeficiency virus protease inhibitors. Jour. Infect. Diseases 1999; 180:448-453. (2). Atzori C, Angela I, Mainini A, Agostini F, Micheli V, and Cargnel A. In Vitro activity of human immunodeficiency virus protease inhibitors against Pneumocystis carinii. Jour. Infect. Diseases 2000; 181:1629-1634. Competing interests: None declared |
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Nicholas D. Chester, postdoctoral fellow Harvard Medical School 77 Avenue Louis Pasteur Boston, Massachusetts 02115
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Peter Flegg has outlined his views on why HAART is beneficial to immunocompromised patients with HIV infection. Indeed, studies such as EuroSIDA (1) indicate a lowered incidence of AIDS-defining illnesses (ADIs) as well as an increase in CD4 counts for patients on HAART as compared to those on other regimens or not taking any antiretrovirals (ARVs). So, the explanation that inhibition of HIV replication results in CD4 count increase, restoration of immune function and greater resistance to opportunistic infections seems to be irrefutable. However, things are never as straightforward as they seem. HAART components are DNA chain terminators and aspartyl protease inhibitors. They have the potential to act against the same enzymes that all organisms and many viruses, including HIV share. Therefore, due to daily consumption for months or years, HAART may work as prophylaxis against microorganisms due to direct activity. Etienne de Harven listed two examples of opportunistic microbes, Candida albicans and Pneumocytis carinii causing thrush and PCP respectively, which are inhibited by HIV protease inhibitors in vitro (2,3). Indeed, another example of a protease inhibitor acting upon a microbe causing disease in AIDS patients is that of indinavir on cryptosporidiosis caused by Cryptosporidium parvum. In fact, based on in vivo and in vitro models, the authors suggested, “Protease inhibitors (PIs) could be considered as good candidates for the treatment of cyptosporidiosis in immunosuppressed persons” (4). This list could continue to grow. How does HIV deplete CD4 cells when it only infects a small fraction of them? Likewise, how does inhibition of HIV, which productively replicates in 1/1000 T cells (5,6,7) by ARVs cause a multi-fold increase in CD4 titers? The HAART protease inhibitors indinavir and saquinavir have been shown to have direct effects on cultured T-cells from HIV infected patients or healthy controls, resulting in cell cycle block, lymphoproliferative response inhibition and decrease in apoptosis (8, 9). The authors from one of the studies concluded, “In individuals on PI therapy, PI-mediated effects could potentially modulate immunologic responses independently of antiviral activity against HIV” (8). A review of immunologic effects of PIs that occur independently of HIV replication is given by Phenix et al. (10). The list of disconnections between virologic and immunologic responses with HAART use may also continue to grow. The use of an inhibitor to further a scientific argument in biology is classic. However, in the case of HAART and HIV/AIDS an important control has never been performed. If Peter Flegg and the orthodoxy wish to argue that HIV replication inhibition is responsible for a linear cascade of downstream effects, it must be shown that the effects are not nonspecific. The best control would be to evaluate the effects of HAART on people with CD4 immunodeficiency who don’t have HIV. For a variety of reasons, it is unlikely that this control can or will be performed. However, an interpretation of a result obtained with the use of HAART that makes assumptions in the absence of control data is both incomplete and unreasonably optimistic. Peter Flegg stated, “The simplest explanation is usually the best (remember William of Occam and his principle of parsimony?) – namely that HIV causes immunodeficiency, and that HAART suppresses HIV and this results in immune recovery.” Actually, this is not the most parsimonious explanation to explain HAART effects. The most simple proposal is that HAART drugs produce their effects through direct action. Direct antimicrobial and immunologic responses to HAART represents the most straightforward explanation to explain its beneficial activity. 1. MocroftId A, Katlama C, Johnson AM, Pradier C, Antunes F, Mulcahy F, Chiesi A, Phillips AN, Kirk O, and Lundgren JD. AIDS across Europe, 1994-98: the EuroSIDA study. Lancet. 2000; 356(9226):291-6. 2. Cassone A, De Bernardis F, Torosantucci A, Tacconelli E, Tumbarello M and Cauda R. In vitro and In Vivo anticandidal activity of human immunodeficiency virus protease inhibitors. Jour. Infect. Diseases 1999; 180:448-453. 3. Atzori C, Angela I, Mainini A, Agostini F, Micheli V, and Cargnel A. In Vitro activity of human immunodeficiency virus protease inhibitors against Pneumocystis carinii. Jour. Infect. Diseases 2000; 181:1629- 1634. 4. Mele R, Gomez Morales MA, Tosini F, Pozio E. Indinavir reduces Cryptosporidium parvum infection in both in vitro and in vivo models. Int J Parasitol. 2003; 33(7):757-64. 5. Ascher MS, Sheppard HW, Anderson RW, Krowka, JF, and HJ Bremermann. Paradox remains. Nature 1995; 375:196 6. Anderson RW, Ascher MS, Sheppard HW. Direct HIV cytopathicity cannot account for CD4 decline in AIDS in the presence of homeostasis: a worst-case dynamic analysis. J Acquir Immune Defic Syndr Hum Retrovirol. 1998; 17(3):245-52. 7. Duesberg P and Bialy, H. HIV an illusion. Nature 1995; 375:197 8. Chavan S, Kodoth S, Pahwa R, and Pahwa S. The HIV protease inhibitor Indinavir inhibits cell-cycle progression in vitro in lymphocytes of HIV- infected and uninfected individuals. Blood 2001; 98(2):383-9. 9. Lu W, and Andrieu JM. HIV protease inhibitors restore impaired T-cell proliferative response in vivo and in vitro: a viral-suppression- independent mechanism. Blood 2000; 96(1):250-8. 10. Phenix BN, Cooper C, Owen C, and Badley AD. Modulation of apoptosis by HIV protease inhibitors. Apoptosis 2002; 7(4):295-312. Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool, UK, FY3 8NR
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Nicholas Chester correctly points out that protease inhibitors have been shown to have some immunomodulatory effects independent of their anti -retroviral action. He also correctly points out that the pathogenesis of CD4 depletion in HIV disease remains somewhat unclear (but HIV mediates its effects on the immune system in several ways, and not purely by a direct cytopathic action), and that the precise nature of T cell reconstitution with HAART is also unclear. These continue to be fruitful areas for ongoing HIV research. However, it would be wrong to jump to the conclusion that the orthodox models of HIV-induced pathogenesis are therefore invalid. While the orthodox model is incomplete, it posesses far fewer "failings" than any of the alternatives. I cannot rule out the possibility that protease inhibitors contribute to immunological (and therefore clinical) recovery, but there are other pertinent reasons to suggest there is little clinically significant benefit. Firstly, in cases of protease-induced HIV resistance there is a normally a steep decline in CD4 lymphocyte count (despite the continued use of the drug). Secondly, we know that susceptibility to opportunistic infections in this scenario correlates not with the continued use of a protease inhibitor, but the CD4 lymphocyte count. If proteases themselves had substantial benefit, they would demonstrate this clearly in cases of clinical drug failure. (There are recent data suggesting that it is probably more beneficial to continue with a failing regimen that to discontinue therapy entirely, but this effect seems modest, and seems to relate to a degree of ongoing viral suppression, albeit suboptimal.) In addition, I can find no evidence that non-nucleosides (which now form the mainstay of therapy, rather than proteases) have any direct anti- microbial or immunological effects. Indeed, considering the mechanism of their action, which is specifically targeted to RT inhibition by a mechanism independent of any potentially non-specific action on cellular enzymes, it seems unlikely that they might be shown to possess this. (However this does not rule out the possibility, I freely admit!). Generally speaking, immune recovery is similar for both protease-based and NNRTI-based regimens, although some differences may be noted (1). (1) Barreiro P, Soriano V, Casas E, Gonzalez-Lahoz J. Different degree of immune recovery using antiretroviral regimens with protease inhibitors or non-nucleosides. AIDS 2003;17(3):447-8 Competing interests: None declared |
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David Rasnick, Visiting Scholar, Dept. MCB, UC Berkeley Berkeley, CA 94720
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HAART: One foot on the gas pedal, the other on the brake! It is often claimed, but rarely documented, that HAART has Lazarus- like effects in some truly sick patients. However, as the members of South African President Thabo Mbeki's AIDS Advisory Panel learned in July 2000, the few miraculous results rarely last more than a few weeks. In arguing the benefits of the HIV protease inhibitors, Peter Flegg fails to take into consideration standard of care requires that combinations of anti-HIV drugs be administered to HIV positive people. All of these drugs are toxic, with many different (and largely unknown) mechanisms of toxicity. That's why there are conferences devoted solely to the toxicity of the anti-HIV drugs. Any serendipitous clinical benefits of individual components of HAART are quickly offset by the toxic effects of the combination of drugs prescribed for life. This explains Flegg's statement that, "in cases of protease-induced HIV resistance there is a normally a steep decline in CD4 lymphocyte count (despite the continued use of the drug). Secondly, we know that susceptibility to opportunistic infections in this scenario correlates not with the continued use of a protease inhibitor, but the CD4 lymphocyte count. If proteases [inhibitors] themselves had substantial benefit, they would demonstrate this clearly in cases of clinical drug failure." Whatever the therapeutic benefits that HIV protease inhibitors may have against yeast and PCP, they are quickly and inevitably overwhelmed by the bone marrow-crushing, liver-destroying, nerve-frying, muscle- wasting, gut-wrenching, metabolism-wreaking effects of HAART. David Rasnick Member of the South African Presidential AIDS Advisory Panel Competing interests: None declared |
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Eleni Papadopulos-Eleopulos, Biophysicist 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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We agree with Nicholas Chester’s view (rapid response “Cause of beneficial effects of HAART potentially misinterpreted”, 2nd April 2004) that the beneficial effect of HAART, if any, may be independent of their effect on “HIV”. Here are a few points in support of his view: 1. HAART affects neither transcription of proviral DNA nor translation of “HIV” RNA into proteins but only decreases infection of new cells. That is, HAART decreases the proviral DNA. In other words, the effect of HAART on the “HIV” RNA is indirect, it is via DNA. For HAART to decrease the “HIV” RNA, it must first decrease its DNA which is not the case. (1) The fact that HAART does not affect the “HIV” DNA means that the treatment has no anti-“HIV” effect. The lack of correlation between the DNA and the viral load means that either the “viral load” test does not measure “HIV” RNA or HAART masks the tests. 2. The conclusion that “HIV” infects only a small fraction of T4 cells was reached following Gallo et al experiments in 1984 (2). Because their hybridisation bands were “faint”, “low signal”, they concluded either that a very small number of T4 cells were infected, or that the results were due to cross-hybridisation with other retroviruses such as HTLV-I or HTLV-II. However, at a 1994 meeting held in Washington sponsored by the US National Institute of Drug Abuse, Gallo admitted "We have never found HIV DNA in the tumor cells of KS...In fact we have never found HIV DNA in T-cells".(3) 3. Although no effort has been spared, to date nobody, not even Gallo’s and Montagnier’s groups, have been able to present evidence which proves that “HIV” kills the T4 cells either directly or indirectly by apoptosis or by any other mechanism. In fact, no evidence exists that “HIV” decreases the T4 cells either by killing, sequestration, or by CD4 down regulation. (4) 4. It is also prudent to note that at least one “anti-HIV” drug, AZT, raises the level of T4 cells, sometimes dramatically, in individuals who are not “HIV infected”. (5) References 1. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Alfonso H, Page B, Causer D (2000). Questions about Results Reported with Potent Antiretroviral Therapy for Human Immunodeficiency Virus Type 1 Infection. J. Infectious Disease 181: 1518-1519. 2. Shaw GM, Hahn BH, Arya S, Groopman, JE, Gallo, RC, Wong-Staal, F (1984). Molecular characterization of human T-cell leukemia (lymphotropic) virus type III in the acquired immune deficiency syndrome. Science 226:1165-1171. 3. Lauritsen JL (1995). NIDA meeting calls for research into the poppers-Kaposi's sarcoma connection. In: Duesberg PH, eds. AIDS: Virus- or Drug Induced. London: Kluwer Academic Publishers, pp. 325-330. 4. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Hedland-Thomas B, Page B (1995). A Critical Analysis of the HIV-T4-Cell- AIDS Hypothesis. Genetica 95: 5-24. 5. Milazzo L, Vaira LM, Cremoni L. CD4+ lymphocyte count variations in HIV- negative subjects treated with zidovudine. AIDS 1996;10:1444-5. Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool, UK, FY3 8NR
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For years we have had to listen to the Perth Group chant their sacred mantra that zidovudine is nothing but a toxic poison that destroys white blood cells (thereby causing “AIDS”). Now they would have us believe (because it conveniently suits their argument of the moment) that zidovudine actually does the opposite and can dramatically raise levels of T lymphocytes. Well which is it? Am I alone in becoming fed up with hearing them refer to research taken entirely out of context, cite hearsay as fact, misquote statements, reinterpret evidence, and prevaricate or worse in order to champion their standpoint while they ignore overwhelming evidence that is contrary to their own view? As another typical example I give you the Perth Group assertion that: “Although no effort has been spared, to date nobody, not even Gallo’s and Montagnier’s groups, have (sic) been able to present evidence which proves that “HIV” kills the T4 cells either directly or indirectly by apoptosis or by any other mechanism.” There is an abundance of experimental research to demonstrate these facts. I remain at a loss to know what the Perth Group define as “proof”, but I am sure by their definition we might just as well declare there is no evidence that proves bacteria cause meningitis. Have the Perth Group never opened a scientific journal, or performed the simple act of a Medline search before? A quick PubMed search that I performed on apoptosis induced by HIV threw up what I initially thought was a total of 80 references. Somewhat discouraged by the thought of chasing up so many articles, I checked again, to find that there were not 80 references, but 80 pages of references numbering 1589 in total. Perhaps I might point the Perth Group to just three of these, each of which provides plenty of evidence (1,2,3). The first review article (with its 315 references) is even available in full text on line with the link below (this should simplify matters for those who do not know how to find research articles) and I defy anyone to read through it and conclude “there is no evidence which proves apoptosis”. I leave it for BMJ readers to decide for themselves whether to believe the Perth Group’s somewhat empiricist concepts of evidence and proof, or to concur with what is accepted by the rest of the scientific community. (1) Andrew D. Badley, André A. Pilon, Alan Landay, and David H. Lynch Mechanisms of HIV-associated lymphocyte apoptosis Blood, 1 November 2000, Vol. 96, No. 9, 2951-2964 http://www.bloodjournal.org/cgi/content/full/96/9/2951 (2) Ross TM. Using death to one's advantage: HIV modulation of apoptosis. Leukemia. 2001 Mar;15(3):332-41 (3) Douek DC. Disrupting T-cell homeostasis: how HIV-1 infection causes disease. AIDS Rev. 2003 Jul-Sep;5(3):172-7. Competing interests: None declared |
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Alexander H Russell, Writer/artist/philosopher WC1N 1PE
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Peter Flegg states: "For years we have had to listen to the Perth Group chant their sacred mantra...Am I alone in becoming fed up with hearing them refer to research taken entirely out of context, cite hearsay as fact, misquote statements, reinterpret evidence, and prevaricate or worse in order to champion their standpoint while they ignore overwhelming evidence that is contrary to their own view? " Yes: you are alone because there is no "overwhelming evidence" that is contrary to their view - and never has been and never will be - because to date 'HIV' has never been proven to be an isolated, sexually transmitted retrovirus. Flegg goes on: "As another typical example I give you the Perth Group assertion that: 'Although no effort has been spared, to date nobody, not even Gallo’s and Montagnier’s groups, have (sic) been able to present evidence which proves that 'HIV' kills the T4 cells either directly or indirectly by apoptosis or by any other mechanism.' There is an abundance of experimental research to demonstrate these facts." What so-called facts'? Please can Flegg produce this "abundance of experimental research to demonstrate these facts"? Just one paper will do and please could Flegg demonstrate its veracity. Where are the real references proving 'HIV' isolation and existence out of over 200,000 papers? There are none! Flegg goes on further regarding so-called 'facts' on the non- isolated ‘HIV’: "I checked again, to find that there were not 80 references, but 80 pages of references numbering 1589 in total." In fact, there are more than 200,000 published referenced papers on ‘HIV’ pseudoscience, which Flegg could cite; however, if the basic premise behind them all is totally false then they are all worthless. Flegg assumes that 'HIV' is an isolated 'retrovirus' (and therefore exists) because he mistakenly and surprisingly naively takes on trust the flawed papers and references in Nature, Science, New Scientist and The Lancet. I leave it for BMJ readers to decide for themselves whether to believe Flegg’s uncritical and reactionary readings of conservative 'consensus science'. The only people who have ever progressed the course of science are those who have questioned and overthrown the prevailing (and invariably false) 'consensus view'. Paul Valery reminds us: "What has been believed by all, always and everywhere, has every likelihood of being untrue." If Flegg has such an abundance of so-called ‘facts’ can he show us a visual image of isolated/purified (uncontaminated) ‘HIV’? Hans Gelderblom of Berlin's Robert Koch Institute co-authored the first paper in Virology, March 1997, showing 'purified HIV' to be 'purified microvesicles'. What was assumed to be 'purified HIV' was in fact "an excess of vesicles" - particles of cellular proteins. The hypothetical 'HIV' is in fact a collection of endogenous microvesicles and cellular proteins (which also never seem to form particles - so how can they be infectious)? Cell-free viral 'HIV' particles have never ever been visualised in any freshly donated bodily fluid including semen, blood, etc. 'HIV' has never ever proven to be a sexually transmitted retrovirus. ‘HIV’ does not exist. Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool, UK FY3 8NR
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I recommend Alex Russell reads both the Perth Group letter of 6th April and my specific response again. In his rush to get his thoughts to “press”, he has totally misread and misunderstood the points being discussed. The Perth Group claimed there was no evidence for HIV-induced apoptosis. My mention of 1589 Pubmed references on the subject refers only to HIV apoptosis, and NOT to references for HIV in general. Again, I challenge him to read just one article on this (1) and conclude that there is no evidence supporting HIV-apoptosis. However, since Alex Russell has moved the goal posts onto the subject of “where is the proof for HIV?”, might I remind him that 8 years ago Professor Peter Duesberg, once renowned as the dissidents’ darling and widely viewed by them as the acceptable face of denialism, specifically replied to Russell’s challenge. In the process Duesberg tried to claim the “£25,000 reward” Russell had offered for proof of the missing HIV. However, considering Russell’s intransigence on the topic of HIV and the fact that he acts as the arbiter of proof rather than an independent panel of scientists, I am not surprised Duesberg failed to collect his due “reward”. Perhaps I could jog Russell’s memory by quoting from Peter Duesberg’s article (2): “In conclusion: HIV has been isolated by the most rigorous method science has to offer. An infectious DNA of 9.15 kilo bases (kb) has been cloned from the cells of HIV-antibody-positive persons, that -upon transfection- induces the synthesis of an unique retrovirus. This DNA "isolates" HIV from all cellular molecules, even from viral proteins and RNA. Having cloned infectious DNA of HIV is as much isolation of HIV as one can possibly get, it is like isolating the fifth symphony from an orchestra hall by recording it on a CD. The retrovirus encoded by this infectious DNA reacts with the same antibodies that crossreact with Montagnier"s global HIV standard, produced by immortal cell lines in many labs and companies around the world for the HIV-test. This confirms the existence of the retrovirus HIV. The uniqueness of HIV is confirmed by the detection of HIV-specific DNA sequences in the DNA of most antibody-positive people. The same DNA is not found in uninfected humans, and the probability to find such a sequence in any DNA sample is 1/49500 - which is much less likely than to encounter the same water molecule twice by swimming in the Pacific ocean every day of your life. The existence of an unique retrovirus HIV provides a plausible explanation for the good (not perfect) correlation between the existence of HIV DNA and antibodies against it in thousands of people that have been subjected to both tests.” I disagree with the Pacific ocean odds analogy, but I have yet to see a coherent response to Deusberg from the dissident lobby. Instead the Perth Group keep parroting their decade-old, discreditied assertions, failing to acknowledge that science in general, and virology in particular, have moved on. Russell also refers to an article by Hans Gelderblom, incorrectly inferring that Gelderblom showed “purified HIV” to be nothing but “purified microvesicles” (3). This is a complete misinterpretation of the paper. Perhaps the actual title of the paper would give Russell a clue as to its content – that microvesicles are a contaminant of gradient-enriched HIV preparations- (and not that HIV does not exist). Gelderblom has published widely in the field of HIV morphology. He has never disputed the existence of HIV, and has produced comprehensive articles detailing HIV’s ultrastructure (which incidentally contain several pictures of HIV virions) (4). The article that Russell has deliberately misquoted is an analysis of showing that if gradient-enrichment is used to isolate HIV, significant contamination with microvesicles occurs because they band at a similar density, with HIV budding co-localising with membrane vesicles (hardly surprising, considering the process of HIV replication and maturation). On EM the vesicles were clearly distinguishable from the 100nm HIV particles and although several antigens are expressed in common, there were several specific to either HIV or to cellular vesicles. Perhaps I should not be too critical of Russell – he is merely doing what many dissidents do, namely regurgitating references to scientific material of which they show little understanding. These articles are often copied from another source such as an HIV dissident web site that has twisted the interpretation of the paper to suit its own ends. (1) Andrew D. Badley, André A. Pilon, Alan Landay, and David H. Lynch. Mechanisms of HIV-associated lymphocyte apoptosis. Blood, 1 November 2000, Vol. 96, No. 9, 2951-2964. http://www.bloodjournal.org/cgi/content/full/96/9/2951 (2) Deusberg, P. 1996. http://www.duesberg.com/papers/continu2.html (3) Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virology. 1997 Mar 31;230(1):125-33. (4) Gelderblom, HR. Fine Structure of HIV and SIV. http://www.hiv.lanl.gov/content/hiv-db/REVIEWS/Gelderblom.html Competing interests: None declared |
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Alexander H Russell, Philosopher/writer/artist WC1N 1PE
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Peter Flegg has a touching faith in the concept of apoptosis and its connection with the hypothetical 'HIV'. However this was merely another desperate attempt by the medical and scientific community to explain cell death in cases of 'AIDS' when all other proposed mechanisms of cell destruction were shown to be wrong. The current situation is that no-one knows why cells are disappearing in PWA's. No mechanism, including apoptosis, has so far been clearly demonstrated to cause the disappearance of T-cells. Even the Devil can quote Duesberg for his own ends. Duesberg's arguments for the isolation of 'HIV' depend entirely on laboratory conjuring tricks using suspect cell lines, mitogenic stimuli etc. which in no way reflect an in vivo situation. Electronmicrographs purporting to show 'HIV' are invariably of particles generated by these artificial methods. To this day no such particles purporting to be 'HIV' have ever been observed under electronmicroscopy in a fresh blood sample or indeed in any body fluid. Flegg does not go on to mention that Duesberg firmly believes that retroviruses are never sexually transmitted - there is not a single recorded case of sexual transmission of retroviruses between animals. Obviously Duesberg believes in the existence of retroviruses and based upon this assumption has become the world's leading authority on retroviruses, so he cannot back-track now and admit that retroviruses probably do not exist. Flegg stated:" Russell also refers to an article by Hans Gelderblom, incorrectly inferring that Gelderblom showed "purified HIV" to be nothing but "purified microvesicles" (3). This is a complete misinterpretation of the paper. Perhaps the actual title of the paper would give Russell a clue as to its content - that microvesicles are a contaminant of gradient- enriched HIV preparations- (and not that HIV does not exist). Gelderblom has published widely in the field of HIV morphology. He has never disputed the existence of HIV." Until 1997, Gelderblom made the common error of accepting the consensus view that material that banded at 1.16 in a sucrose gradient represented purified retrovirus when it was obvious from their own micrograph of material banding at 1.16 consisted of cellular vesicles, debris, etc with one or two little dots indicated by arrows and alleged to be 'HIV'. However, when referring to the figure used in his paper, he still compounded the error by claiming it represented 'purified HIV' when it was obviously grossly contaminated by other matter. How can this represent purified 'HIV' if the majority of the objects in the micrograph are miscellaneous gunge? How can that be pure 'HIV'? This is a typical example of the shoddiness of 'HIV' research that has always been based on arbitrary scientific assumptions that all too often are shown by more recent research to be completely wrong. A perfect example to illustrate this point is to be found in recent developments concerning the role of RNA in cellular biology. Since Crick and Watson's discovery of DNA it has always been assumed that this extended molecule ran the show and that RNA was the mere drudge of the cell, fetching and carrying the all important DNA. Recent developments have shown the role of RNA to be infinitely more important that that of DNA and that the latter is merely an inert molecule used to store genetic information. If DNA is the dictionary, RNA makes use of it - a dictionary cannot write a novel: try telling this to the powers that be and they will hoot with derision or sheer anger! Again, one of the earliest basic assumptions concerning retroviruses was that they were unique in possessing the enzyme reverse transcriptase. From this it was supposed that when reverse trabscriptase activity was detected in a cell sample it was proof that the cells were infected with a retrovirus. However, by the late 1980's, when the lucrative 'HIV' bandwagon was already rolling and all those failed cancer researchers had clambered aboard, nobody wanted to admit that by then it was well known that far from being clear evidence of retrovirus infection, reverse transcription is a common cellular occurrence, found in virtually all plant and mammalian cells; indeed, reverse transcription is not even unique to the hypothetical retroviruses as we now know some hepatititis viruses, and from the plant kingdom, the tobacco mosaic virus, also replicate using reverse transcription. Try pinning down any 'HIV expert' on this topic and they shuffle their feet and look at the ground. It will be fascinating to see how much the infant science of micro-RNA technology will further compromise currently held assumptions about cellular biology and help to demolish this whole 'HIV' nonsense. In conclusion might I suggest Flegg remembers the observation of C.H. Waddington, Geneticist (1905-1975): "The most formidable barrier to the advancement of science is the conventional wisdom of the dominant group." The only real advancements in science and medicine are made by people who manage to surmount, or work their way round, that barrier. Too many people, for reasons of ego or financial gain, seek to preserve the status quo, refusing to allow critical thinking and radical change. Flegg seems to believe that if enough people say something it becomes true. As Dr. Kary Mullis, Biochemist, 1993 Nobel Prize for Chemistry said: "If there is evidence that HIV causes AIDS, there should be scientific documents which either singly or collectively demonstrate that fact, at least with a high probability. There is no such document." Mr. Flegg: Kary Mullis is a Nobel Laureate - you are not. In the light of that Kary Mullis quote, what evidence does Flegg have for the assumption that 'HIV' causes 'AIDS'? Association is not proof of causation! Can Flegg show me visual evidence; i.e. in a published electronmicrograph, of massed, purified (isolated from all other contaminants)'HIV' particles found in a fresh blood sample? In 20 years of 'HIV' research no one has ever done this. Why? If Flegg can produce such evidence then I will be convinced. To say that 'HIV' exists even though we cannot see it with all the resources of modern technology is a bit like asking us to believe in the Holy Ghost! Flegg would do well to distinguish between science and theology. Can Flegg prove that 'HIV' exists via visual evidence? Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool, UK, FY3 8NR
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I had hoped that Alex Russell might have taken up my repeated suggestion to read the review article on HIV-induced apoptosis(1). Clearly he has not, or he would attempt to make disparaging comments and sweep the quite unambiguous evidence for its existence under the carpet. His bald (and untrue) statement that "No-one knows why cells are disappearing in patients with AIDS" demonstrates that he is the one putting reliance in faith and not facts. It seems that it is Russell rather than myself who has trouble distinguishing between science and theology. Perhaps he would like to prove me wrong and discuss some of the scientific evidence for HIV -induced apoptosis in more detail, and explain why he thinks the mechanism does not exist? We make scientific advancements by challenging accepted orthodox concepts, and in this I can agree with Russell. What he fails to grasp is that ever since the first recognition of "AIDS", the scientific method has been applied consistently to the problem of HIV. By a process of incremental inductive reasoning we have built up a valid model for the existence and role of HIV. Scientists themselves yearn for new knowledge and horizons, and there are still many things to learn about HIV. The stimulus for this comes from within, and does not depended upon the urgings of "flat-earthers" who challenging the status quo. One example of this can be seen in the very concept he ridicules, HIV -induced apoptosis. The discovery (by orthodox scientists) that fewer CD4 lymphocytes were destroyed directly by HIV that had previously been assumed led directly to the formulation of new hypotheses and the discovery, confirmed by repeatable experimentation, that apoptosis played a major role. This is science in action, and we should celebrate it, not denigrate scientists for changing their minds. It is clear that the "HIV hypothesis" which Russell dismisses has remained valid for nearly 25 years, and has withstood all the challenges thrown at it by the denialists. Russell describes himself as a philosopher. Is it not time for him to embrace the idea espoused by the American philosopher Charles Sanders Peirce, namely that of pragmatism? Finally, I have great distaste for "argument from authority". Would Russell be impressed if I said to him "I am a doctor, you are not"? I very much doubt it. Russell may like to contrast me with Kary Mullis, Nobel Laureate in chemistry and PCR inventor, if he so wishes. Perhaps he will sleep better at night knowing how much this will reinforce his faith in the non-existence of HIV. I am not a Nobel Prize winner and never will be, but not all Nobel laureates are automatically experts outside of their immediate areas of expertise (remember Linus Pauling anyone?). However, Kary Mullis knows less about HIV and its effects than thousands of other equally eminent scientists and doctors, and dare I say it, less than me too. (1). http://www.bloodjournal.org/cgi/content/full/96/9/2951 Competing interests: None declared |
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Alexander H Russell, Philosopher/writer/artist WC1N 1PE
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Peter Flegg states: "It is clear that the ‘HIV hypothesis’ which Russell dismisses has remained valid for nearly 25 years, and has withstood all the challenges thrown at it by the denialists." The announcement that The "probable cause of Aids has been found" was made on April 23rd 1984, making the mistaken, as yet unproven hypotheses, twenty years old. It has remained valid for those opportunistic scientists and lazy doctors who refuse to acknowledge the gaping holes in the theory, and the flawed and shoddy science, which brought it into being. It is also kept in place by those afraid to let the truth come out for fear of negligence suits and loss of prestige and high incomes: while the ‘HIV hypothesis’ has been a financial success for some - it has failed as a scientific paradigm. At the risk of stating the obvious, the hallmark of a successful hypothesis is that predictions based on it will be fulfilled. In the case of the ‘HIV‘ hypothesis, the predictions have all been wrong, always totally off-beam. Despite shoddy attempts to massage the figures by widening the syndrome definition to include diseases such as tuberculosis and vaginal cancer in the list of ‘AIDS defining’ illnesses, just to keep the numbers up, and using differing definitions of the illness in different continents – the African Bangui definition of AIDS does not apply to Main Street USA or Europe – the predicted heterosexual epidemic of AIDS just has not happened. In the USA, recent articles in the New York Times and other august newspapers have pointed this out, posing the question “Where is the heterosexual epidemic?” Britain provides a case in point. Despite a huge level of teenage promiscuity which has resulted in a massive rise in STD’s, and the highest number of unwanted teenage pregnancies in Europe, there has been no commensurate rise in HIV spread. Alarmist headlines about ‘recent figures’ showing an increase in heterosexual AIDS, when examined in detail using tables published by the Public Health Laboratory Service, reveal that the heterosexual increase is almost totally confined to recent immigrants from Africa, the Caribbean, South America and Asia. These cases account for more than 80% of Britain’s so-called heterosexual cases of HIV positivity. The remainder are practically all male and female IV drug users. There just is no heterosexual ‘HIV/AIDS’ epidemic in the West – Britain’s is imported from abroad. In 1985 the Royal College of Nursing predicted that one million people in Britain "will have AIDS in six years time" yet 15 years later (in 2000) AIDS deaths had totalled 263 - less than the number of people who died from falling down stairs. Peter Flegg repeats the comparison of AIDS rethinkers with ‘flat earthers’. This insult is singularly inept. He should remember that originally the entire population was misled by the then keepers of the received wisdom into believing the world was flat – the status quo. It was the rethinkers, whom Flegg calls "denialists", who fought prejudice and ridicule to prove that what had always been believed was wrong, and that not only was the earth round but that it also revolved around the sun. Today’s "flat earthers" are the AIDS orthodoxy majority, who despite glaringly obvious, gross errors in their thinking still maintain that AIDS is caused by a retrovirus. Twenty years of research, billions of wasted dollars and more than 200,000 scientific papers down the road, and still no-one has published an electronmicrograph showing purified/isolated ‘HIV’, devoid of any other material, recovered from a fresh blood sample. If you can’t see it, it ain’t there – the Emperor has no virus! As Oliver Cromwell might have said to Peter Flegg – "I BESEECH YOU IN THE BOWELS OF CHRIST THINK IT POSSIBLE YOU MAY BE MISTAKEN." Competing interests: None declared |
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Etienne de Harven, Emerit. Prof. Pathol. 06530 St-Cezaire, France
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I simply wish to congratulate Alexander Russel for the PERFECT answer he gave, on April 24, to the non-sense arguments Peter Flegg keeps needling us concerning the highly hypothetical and, so far, totally unproven dogma of the so-called "HIV ". I certainly could not have said it myself in more efficient words. To the best of my analysis of all the published literature, the existence of a so-called "HIV" has never been proven in any scientifically acceptable way. Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool, UK, FY3 8NR
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Recently I have noticed a tendency for some HIV dissidents to compliment each other effusively on the perfection, wit, elegance (or whichever other superlative springs to mind) of their contributions to the HIV debate. I wonder if this marks a new tactic for the dissidents – to indulge in an orgy of mutual backslapping or self-congratulation in the hope that no-one else will notice you have nothing of substance worth saying. Observers in this debate are not likely to be misled. The emperor may cloak himself in the “HIV is a myth” mantle, but his nakedness is obvious despite the sycophantic expressions of wonderment from his dissident courtiers. Competing interests: Possession of the rapidly fading hope that Alex Russell will eventually tell us why he thinks HIV-induced apoptosis is a myth. |
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Alexander H Russell, Philosopher/artist/writer WC1N 1PE
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Dr. Peter Flegg's dogged belief in 'HIV-induced apoptosis' is really rather endearing. Any drowning man is entitled to clutch at a straw, and this is obviously Dr. Flegg's. His 'rapidly fading hope' must be revived, even if in the process I must apply a lighted match to both ends of said straw, and two reasons will suffice to demolish his ridiculous claims on behalf of 'HIV' as the cause of cellular suicide. 1. In a different but analogous context, Peter Duesberg explained why 'HIV' cannot be cytotoxic. He pointed out that 'HIV' is regularly replicated for research purposes in T4 cells, just those very cells the virus is supposed to destroy, with no observable damage to those cells. If 'HIV' induces apoptosis in T4 cells, this would have been noticed in this context. 2. Subsequently, Luc Montaigner, the leader of the team alleged to have discovered 'LAV/HIV', added 'HIV' to a T4 cell culture and observed the expected destruction of the cells. However, when he decided to add a powerful antibiotic - doxycycline - to the culture, the cells stopped dying, and continued to produce virus without mishap. He naturally reasoned that since antibiotics cannot kill a virus, the culture must have contained some other cytotoxic micro-organism, and sure enough closer examination revealed that the culture was contaminated with an ubiquitous bacterium called mycoplasma. Once the antibiotic had eradicated this contaminant, the cells continued to divide under mitogenic stimulation as usual, and to produce alleged virus. If, as Flegg supposes, 'HIV' induces apoptosis, then the cells should have died with or without mycoplasma, and with or without any antibiotics. What is beyond any doubt is that many recreational drugs, as well as the so-called 'antiretrovirals' prescribed for those deemed to be infected with 'HIV', are highly cytotoxic and are far more likely to be the true cause of what is now being misinterpreted as 'HIV-induced apoptosis'. As I have now satisfied his monotonous demands for an explanation of why I think "that HIV-induced apoptosis is a myth" perhaps he could return the complement and explain why no one has ever succeeded in producing visible evidence of the myriad 'HIV' viral particles alleged to be teeming in the blood and other bodily fluids of people who test 'positive' for antibodies supposedly against 'HIV' proteins. Seeing is believing. If 'HIV' is there, as Flegg naively supposes, why has it never been shown using electronmicroscopy? Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool, UK. FY3 8NR
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Alex Russell may find my belief in “HIV-induced apoptosis” endearing. At least I am in excellent company. He still has not read the review on apoptosis that I recommended to him and given any credible scientific evidence for his (and the Perth Group’s) claim that it is a myth, despite overwhelming evidence for its existence as a mechanism for CD4 lymphocyte depletion during the course of HIV infection (1). The trite “reasons” he gives to justify his out-of-hand dismissal do not even hold up to cursory examination. Perhaps he can elaborate further on why he specifically rules out any apoptotic effect of HIV purely on the basis that lymphocytes can proliferate under the effects of mitogen stimulation? No-one is claiming lymphocyte apoptosis is a universal and instant consequence of infection with HIV - if it were, survival of patients would be measured in weeks and not decades. Russell also seems somewhat confused about the pathogenesis of lymphocyte depletion. Firstly he denies it even occurs (using this as proof that apoptosis therefore cannot exist). However, he later claims it does, blaming anti-retroviral drugs for the phenomenon (he states: “beyond any doubt…the (cytotoxic) anti-retrovirals…are far more likely to be the true cause of what is now being misinterpreted as HIV-induced apoptosis”). This sort of contradiction is typical of the dissident stance – concur with whatever seems to support your dogma and ignore any glaring inconsistencies. For Russell’s information, HIV drugs do not induce CD4 lymphocyte apoptosis (or, to put it in his terms, even what we “misinterpret” as apoptosis). In fact HIV drugs across all the classes have been shown to inhibit apoptosis. (2-6). Russell’s attempts to explain away his disbelief in the mechanisms of lymphocyte depletion and apoptosis have certainly not satisfied what he terms my “monotonous demands”. They have merely demonstrated his confusion on the subject. I will spare him the embarrassment of asking him for further clarification – there is little point requesting something that he cannot provide. Is it not time the dissidents stopped automatically claiming that scientific evidence that contradicts their view is a "myth", and provide some real evidence for their claim to the contrary? Finally, Russell asks why HIV has never been shown to exist using electron microscopy. Of course, we know it has, but he will always refuse to accept the evidence of his own eyes, claiming what everyone else sees are “microvesicles” or “contaminants”. This point has been debated ad nauseam in these columns, and further discussion is unlikely to get anywhere. 1. Andrew D. Badley, André A. Pilon, Alan Landay, and David H. Lynch. Mechanisms of HIV-associated lymphocyte apoptosis. Blood, 1 November 2000, Vol. 96, No. 9, pp. 2951-2964 http://www.bloodjournal.org/cgi/content/full/96/9/2951#SEC11 2. Grelli S, D'Ettore G, Lauria F, Montella F, Di Traglia L, D'Agostini C, Lichtner M, Vullo V, Favalli C, Vella S, Macchi B, Mastino A. CD4+ lymphocyte increases in HIV patients during potent antiretroviral therapy are dependent on inhibition of CD8+ cell apoptosis. Ann N Y Acad Sci. 2003 Dec;1010:560-4. 3. Bellet V, Duval R, Delebassee S, Cook-Moreau J, Bosgiraud C. Related Articles, AZT inhibits Visna/maedi virus-induced apoptosis. Arch Virol. 2004 Mar;149(3):583-601. Epub 2003 Oct 30. 4. Cooper CL, Phenix B, Mbisa G, Lum JJ, Parato K, Hawley N, Angel JB, Badley AD. Antiretroviral therapy influences cellular susceptibility to apoptosis in vivo. Front Biosci. 2004 Jan 1;9:338-41. 5.Ghibelli L, Mengoni F, Lichtner M, Coppola S, De Nicola M, Bergamaschi A, Mastroianni C, Vullo V. Anti-apoptotic effect of HIV protease inhibitors via direct inhibition of calpain. Biochem Pharmacol. 2003 Oct 15;66(8):1505-12 6. Pilon AA, Lum JJ, Sanchez-Dardon J, Phenix BN, Douglas R, Badley AD. Induction of apoptosis by a nonnucleoside human immunodeficiency virus type 1 reverse transcriptase inhibitor. Antimicrob Agents Chemother. 2002 Aug;46(8):2687-91. Competing interests: None declared |
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Peter Flegg, Consultant physician Blackpool, UK FY3 8NR
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In my last response to Alex Russell I stated HIV drugs inhibited and did not induce CD4 lymphocyte apoptosis. As a point of clarification, I think I should point out that HIV drugs have been shown to cause apoptosis in some other cell lines (PBMCs), albeit in the absence of HIV infection (1). The 6th reference I cited in my response also referred to this phenomenon (2). 1. Viora M, Di Genova G, Rivabene R, Malorni W, Fattorossi A. Interference with cell cycle progression and induction of apoptosis by dideoxynucleoside analogs. Int J Immunopharmacol. 1997 Jun;19(6):311-21. 2. Pilon AA, Lum JJ, Sanchez-Dardon J, Phenix BN, Douglas R, Badley AD. Induction of Apoptosis by a Nonnucleoside Human Immunodeficiency Virus Type 1 Reverse Transcriptase Inhibitor. Antimicrob Agents Chemother. 2002 Aug;46(8):2687-91. Competing interests: None declared |
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Alexander H Russell, Philosopher/writer/artist WC1N 1PE
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Peter Flegg stated: "Finally, Russell asks why HIV has never been shown to exist using electron microscopy. Of course, we know it has..". We know nothing of the kind! All Peter Flegg needs to do to prove his point is quote a single paper containing an eletronmicrograph depicting massed 'HIV' particles, devoid of any other contaminant material, recovered from a fresh blood sample – standard procedure in proving the existence of a novel virus. No such evidence yet exists for 'HIV'. I challenge him to produce it. Unless or until he can, he has lost the plot and the argument. Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool UK, FY3 8NR
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I suggest that if Russell spends some time reading previous responses in the BMJ debates on HIV he may find the information he seeks. His antiquated definitions of what constitute viral identification and isolation do not apply in current molecular virology. Brian Foley's responses to the Perth Group (and his analogy with computer viruses) should prove enlightening. (http://bmj.bmjjournals.com/cgi/eletters?lookup=by_date&days=1#58034) Competing interests: None declared |
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Eleni Papadopulos-Eleopulos, Biophysicist 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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Re: Perth Group misinterpretations
In his rapid response “Perth Group misinterpretations” 9th April 2004, Peter Flegg wrote: “For years we have had to listen to the Perth Group chant their sacred mantra that zidovudine is nothing but a toxic poison that destroys white blood cells (thereby causing “AIDS”). Now they would have us believe (because it conveniently suits their argument of the moment) that zidovudine actually does the opposite and can dramatically raise levels of T lymphocytes.”
In our paper “A Critical Analysis of the Pharmacology of AZT and its Use in AIDS” (1) www.theperthgroup.com/SCIPAPERS/cmroazt.html we discuss AZT toxicity, give a mechanism for it, and thus a way of preventing and reversing it. However, our paper concentrated on the efficacy of AZT and noted that: (i) all the “HIV” experts agree that only the triphosphorylated form of AZT (AZTPP) and not the unphosphorylated form administered to patients is the active agent; (ii) “According to the 1997 British HIV Association guidelines for antiretroviral treatment of HIV seropositive individuals, ‘If the viral load has not fallen by about 1 log 8–12 weeks after treatment initiation consideration should be given to modify therapy’”(2) “In their 1996 paper in Nature Medicine, Saag, Shaw, Coombs and their associates stated that ‘A three-fold or greater sustained reduction (> 0.5 log) of the plasma HIV RNA levels is the minimal response indicative of an anti-viral effect...return of HIV RNA levels to pretreatment values (or to within 0.3–0.5 log of the pretreatment value), confirmed by at least two measurements, is indicative of drug failure’.” (3)
We have presented evidence that: (i) there is no AZT triphosphorylation in vivo; (ii) AZT has no effect on the “viral load” or any other “HIV” parameter;
and concluded that the clinical and immunological effects of AZT, if any, must result from AZT acting in ways other than as an antiretroviral drug. (1) The fact that AZT raises the level of T4 cells in individuals who are not “HIV infected” lends support to this conclusion.
Would please Peter Flegg read our AZT paper (1) and tell us where we are wrong?
In our rapid response “Re: Cause of beneficial effects of HAART potentially misinterpreted” 6th April 2004, we wrote: “4. It is also prudent to note that at least one “anti-HIV” drug, AZT, raises the level of T4 cells, sometimes dramatically, in individuals who are not “HIV infected”.” And not “can dramatically raise levels of T lymphocytes” as Peter Flegg wrote.
Raising or decreasing the T4 cells is not synonymous with raising or decreasing the “levels of T lymphocytes”.(4)
We note that Peter Flegg responded to our 4th point that we made in our rapid response.
Since points 1 to 2 address much more fundamental issues, would please Peter Flegg tell us where we are wrong and why?
Peter Flegg wrote: “As another typical example I give you the Perth Group assertion that: “Although no effort has been spared, to date nobody, not even Gallo’s and Montagnier’s groups, have (sic) been able to present evidence which proves that “HIV” kills the T4 cells either directly or indirectly by apoptosis or by any other mechanism.” There is an abundance of experimental research to demonstrate these facts. I remain at a loss to know what the Perth Group define as “proof”, but I am sure by their definition we might just as well declare there is no evidence that proves bacteria cause meningitis.”
Peter Flegg quoted only part of our point 3, we wrote: “Although no effort has been spared, to date nobody, not even Gallo’s and Montagnier’s groups, have [ the “(sic)” was Peter Flegg’s insertion] been able to present evidence which proves that “HIV” kills the T4 cells either directly or indirectly by apoptosis or by any other mechanism. In fact, no evidence exists that “HIV” decreases the T4 cells either by killing, sequestration, or by CD4 down regulation. (4)”
If Peter Flegg had read our reference 4, he would have discovered that our statement he quoted is supported by evidence presented there. So would Peter Flegg please tell us why he criticised our statement without referring or responding to our paper which contains the evidence supporting our view?
Since Peter Flegg hasn’t read our reference, here are two salient quotes taken from it: (The complete paper is at www.theperthgroup.com/SCIPAPERS/ept4cells.html )
“Using MCA [monoclonal antibodies] for serial measurement of CD4 and CD8 expressing lymphocytes in mitogenically stimulated HIV infected cultures, it has been shown that in cultures prepared such that the majority (>95%) of lymphocytes are purified T4 cells, there is a progressive disappearance of CD4 expressing cells. This observation was interpreted by Gallo and others "that HTLV-III has a cytopathic effect on OKT4-positive (OKT4+) cells" (Fisher et al., 1985). However, according to Klatzmann, Montagnier and other French researchers "this phenomenon could not be related to the cytopathic effect" of HIV but is "probably due to either modulation of T4 molecules at the cell membrane or steric hindrance of antibody-binding sites" (Klatzmann et al., 1984a Klatzmann et al., 1984b). That is, the decrease in T4 cells is not due to destruction of cells but due to a decrease in MCA binding to their surface. Nevertheless, the above data were interpreted as evidence for selective infection and killing of T4 cells by HIV, and together with the fact that "we knew of no agents, aside from a family of human T- lymphotropic retroviruses that we had discovered three years earlier and named human T-cell leukaemia (lymphotropic) virus (HTLV), that demonstrated such tropism to a subset of lymphocytes", was presented as one of two arguments in support of the HIV hypothesis of AIDS (Gallo et al., 1985). (The other argument was based on the perceptions that AIDS was a new disease and the epidemiology was consistent with an infectious cause).
However:
(a) HIV cultures/co-cultures are stimulated with such oxidising agents as PHA, ConA, radiation, PMA, polybrene and IL-2;
(b) these agents at relatively low concentration can induce decrease in CD4 expressing cells, in the absence of HIV (Acres et al., 1986; Hoxie et al., 1986; Zagury et al., 1986; Scharff et al., 1988), without killing T4 cells.
(c ) in 1986, Zagury, Gallo and their associates (Zagury et al., 1986), prepared T-cell cultures (which contained 94% CD4+ cells), from normal donors. Cultures were stimulated with PHA and were (i) "infected" with HIV;
(ii) left uninfected.
Control cultures remained both unstimulated and uninfected. After 2 days of culture, the proportion of CD4+ cells in the stimulated-uninfected and stimulated-infected cultures was 28% and 30% respectively, while at 6 days the number was 10% and 3%; the controls not changing significantly.
Thus, HIV is not necessary for the disappearance of CD4 expressing cells, as measured by the use of MCA in "HIV infected" stimulated cultures. The stimulants can induce the effect in the absence of "HIV". Furthermore, the decrease in T4 cells may not be due to destruction of T4 cells but to a decrease in the number of cells binding MCA.” “Despite all these data, consensus still prevails that HIV infection leads to a "quantitative decrease in the TH-cell population that will lead to acquired immune deficiency syndrome (AIDS)" (Ameisen & Capron, 1991) [TH=T4]. However, no agreement exists as to the mechanism by which HIV kills T4 cells.
According to Claude Ameisen and André Capron from the Pasteur Institute, not one of the mechanisms "proposed to account for these TH-cell defects, including: (1) immune suppression, or its opposite, hyperactivation and exhaustion of the TH cells, (2) inhibitory signals mediated by HIV viral or regulatory gene products, (3) autoimmune responses, (4) selective infection and destruction of memory TH cells, (5) syncytia formation between infected and uninfected cells, and (6) inappropriate immune killing of uninfected cells", is satisfactory.
Instead, in 1991 they put forward the hypothesis "that a single unique mechanism, activation-induced T-cell death [also known as programmed cell death (PCD) or apoptosis] can account for both the functional and numerical abnormalities of T4 cells from HIV infected patients...We propose that the simplest explanation of TH-cell defects leading to AIDS is that HIV infection leads to an early priming of TH cells for a suicide process upon further stimulation. In HIV infected patients, circulating gp120, gp120-antibody immune complexes or anti-CD4 autoantibodies, that all bind CD4, may represent appropriate candidates for the priming of T cells for a PCD response following activation" (Ameisen & Capron, 1991). In support of their theory they reported that stimulation of peripheral blood mononuclear cells (PBMC) of asymptomatic HIV infected individuals with pokeweed mitogen (PWM) or staphylococcal enterotoxin B (SEB), "was followed by cell death", whereas no death was observed at 48h in the unstimulated cells. Cell death was only observed in the CD4+ enriched population and not in the CD8+ lymphocytes. Cell death was not found in unstimulated or stimulated PBMC from HIV- negative individuals (Groux et al., 1991; Groux et al., 1992). However, to date, "no evidence for circulating soluble gp120 has yet been reported" (Capon & Ward, 1991), or for gp120- antibody immune complexes in AIDS patients. Furthermore, although in the following years, researchers from many institutions published data confirming the apoptotic death of PBMC cultures from HIV infected individuals, their data seem to contradict both Ameisen and Capron's experimental findings as well as their proposed mechanism of HIV induced apoptosis:
1. Addition of anti-gp120 or anti-CD4 monoclonal antibodies (MCA) to HIV infected cultures permitted sustained high levels of viral replication, but blocked apoptosis and cell death (Terai et al., 1991; Laurent-Crawford et al., 1992);
2. Experiments performed on cultures with or without stimulation showed "both CD4+ and CD8+ cells from HIV-infected individuals die as a result of apoptosis" (Meyaard et al., 1992).
In a 1991 paper, published in Virology (Laurent-Crawford et al., 1991), Montagnier and his colleagues showed that:
(a) in acutely HIV infected CEM cultures in the presence of mycoplasma removal agent, cell death (apoptosis) is maximum at 6-7 days post infection, "whereas maximal virus production occurred at Days 10-17"-that is, maximum effect precedes maximum cause;
(b) in chronically infected CEM cells and the monocytic line, U937, no apoptosis was detected although "These cells produced continuously infectious virus";
(c ) in CD4 lymphocytes isolated from a normal donor, stimulated with PHA and infected with HIV in the presence of IL-2, apoptosis becomes detectable 3 days post infection and clearly apparent at 4 days. "Intriguingly, on the 5th day" apoptosis "became detectable in uninfected, PHA stimulated cells". Figure 9, where the data are presented, shows approximately the same degree of "apoptotic events" in the PHA cultures at 5 days as in the PHA+HIV cultures on the 4th day "post infection".
They concluded: "These results demonstrate that HIV infection of peripheral blood mononuclear cells leads to apoptosis, a mechanism which might occur also in the absence of infection due to mitogen treatment of these cells... Interestingly, HIV infection of such mitogen stimulated cells resulted in a slight acceleration of the first signs of apoptosis, thus indicating the intrinsic effect of HIV infection" (Laurent-Crawford et al., 1991).
The conclusion that HIV has an "intrinsic effect" on PCD can be questioned on several grounds:
1. The "slight acceleration of the first signs of apoptosis" in the stimulated HIV infected cultures, as compared to the non-HIV infected stimulated cultures, may not be due to HIV but to the many non-HIV factors present in "HIV" inocula, including:
(a) Mycoplasmas and other infectious agents;
(b) The many cellular proteins present in the "HIV preparation" (Henderson et al., 1987);
(c ) PHA, present in the cultures from which the "HIV preparation" was derived;
2. That HIV is not the cause of apoptosis is also indicated by the fact that in chronically infected cell lines in which virus is continuously produced, apoptosis is not detected;
3. That HIV may play no role in apoptosis is also suggested by the presently accepted mechanism of apoptosis. Apoptosis occurs both in healthy and in pathological conditions, is frequently prominent amongst the proliferating cells of lymphoid germinal centres, and can be enhanced by numerous agents including radiation, cytotoxic drugs, corticosteroids and the calcium ionophore A23187 (Kerr & Searle, 1972; Don et al., 1977; Wyllie et al., 1980; Wyllie et al., 1984). Apoptosis is cellular death characterised by morphological criteria: cellular condensation, DNA fragmentation, and plasma membrane "blebbing" leading to the release of "apoptic bodies" which vary widely in size and some of which contain pyknotic chromatin surrounded by intact membranes (Kerr & Searle, 1972; Don et al., 1977; Wyllie et al., 1980; Wyllie et al., 1984). These changes are thought to be induced by increased concentration of Ca++ which in its turn induces contraction of the cytoskeleton whose main components are known to be the ubiquitous proteins, actin and myosin (Jewell et al., 1982; Cohen & Duke, 1984; McConkey et al., 1988; McConkey et al., 1989; Reed, 1990).
However, evidence exists indicating that intracellular Ca++ concentration and contraction of the actin-myosin system (cellular condensation), are induced by perturbances in the cellular redox state (Papadopulos-Eleopulos et al., 1985; Papadopulos-Eleopulos et al., 1989b). In fact, for more than a decade, evidence has existed showing that oxidising agents, including all mitogenic (activating) agents, can induce: reversible cellular changes; cellular activation; malignant transformation; mitogen unresponsive cells; or cellular death, including death by apoptosis. The ultimate outcome depends on the concentration of the agent, its rate of application, the initial state of the cells and the cellular milieu (See reference (Papadopulos-Eleopulos, 1982)).
More recent data confirm the fact that the intracellular free Ca++ concentration is regulated by the cellular redox state. Oxidation leads to an increased, and reduction to a decreased, Ca++ concentration (Trimm et al., 1986). Cellular surface blebbing (Jewell et al., 1982; Lemasters et al., 1987; Reed, 1990), chromatin condensation (Pellicciari et al., 1983), and apoptosis (Morris et al., 1984) are the direct result of cellular oxidation in general and of cellular sulphydryl groups in particular.”
Note: 1. The author of Peter Flegg’s second reference (see below) wrote: “Studies analyzing the mechanisms responsible for apoptosis in human cells have revealed that the cysteinyl aspartate-specific protease (caspase) family constitutes the effector arm of apoptosis. Caspases are synthesized as inactive pro-enzymes that are activated by upstream proteins in response to an apoptotic stimulus and are characterized by a cysteine located within their active site… One of these proteases, calpain, is a member of the calcium-dependent cysteine proteases and is involved in some forms of apoptosis.” 2. More than a decade after the oxidative theory of AIDS and "HIV" was proposed by our group Montagnier wrote: "A large body of data on in vitro human immunodeficiency virus (HIV) infection and biochemical clinical studies suggests that oxidative stress plays a role in AIDS pathogenesis. Recent reports have implicated intracellular excess of reactive oxygen species (ROS) in the induction of HIV expression and in the initiation of apoptotic cell death. Studies showing a decrease in glutathione in peripheral blood mononuclear cells from symptom-free persons offer further evidence of a metabolic alteration leading to the decreased ability to counteract oxidative stress. In AIDS pathogenesis, oxidative stress is proposed as a metabolic alteration that favours disease progression by inducing both viral replication and apoptotic death." (emphasis ours).” (5)
Peter Flegg wrote: “Have the Perth Group never opened a scientific journal, or performed the simple act of a Medline search before? A quick PubMed search that I performed on apoptosis induced by HIV threw up what I initially thought was a total of 80 references. Somewhat discouraged by the thought of chasing up so many articles, I checked again, to find that there were not 80 references, but 80 pages of references numbering 1589 in total. Perhaps I might point the Perth Group to just three of these, each of which provides plenty of evidence (1,2,3). The first review article (with its 315 references) is even available in full text on line with the link below (this should simplify matters for those who do not know how to find research articles) and I defy anyone to read through it and conclude “there is no evidence which proves apoptosis”. I leave it for BMJ readers to decide for themselves whether to believe the Perth Group’s somewhat empiricist concepts of evidence and proof, or to concur with what is accepted by the rest of the scientific community.”
In the first
reference Peter Flegg cites the authors proposed several “mechanisms of
HIV-associated lymphocyte apoptosis”. In the second, “the validity of the
apoptosis hypothesis in HIV disease and the potential
mechanism(s) that HIV proteins perform in the progressive T cell depletion
observed in AIDS pathogenesis” is discussed. (emphasis ours). In the abstract
of the third reference (we could not access the complete article) one reads: “In
the absence of antiretroviral treatment, HIV-1 establishes a chronic infection
that is marked by the progressive depletion of CD4+ T-cells...Yet the mechanisms
by which this depletion arises remain a matter of controversy. This review will
address what is exceptional about HIV-1 infection that sets it apart from other
viral infections. Recent attempts to understand HIV-1 pathogenesis have set
aside the view that CD4+ T cell depletion is effected solely by HIV-1-mediated
killing in favor of a more complete explanation that also includes T-cell
dynamics and, more specifically, chronic immune activation as a central factor
in HIV-1 pathogenesis”. Although in the first reference, the authors assume that “HIV” causes apoptosis, at the end of this article, one reads: “If CD4 T-cell depletion in HIV infection results from enhanced apoptosis, then the prevention of apoptosis might be expected to modify the cause of HIV disease”. The word “If” means “on the condition or assumption of”. In this context “If” conveys the authors’ view that in their review they do not consider the role of “HIV” in apoptosis as being resolved. In the second reference, the author wrote: “It is now widely appreciated that apoptosis contributes to most types of physiological cell death. However, its participation in the pathological forms of cell death by HIV and other viruses is less fully understood”.
The only way to prove that “HIV” causes apoptosis is to show that the introduction of purified “HIV” in cell cultures or when administered to animals leads to a significant increase of apoptosis as compared to the appropriate controls. It is scientific nonsense to introduce Bess’s or Gluschankof’s “purified HIV” (let alone Montagnier’s “purified virus”), observe an increase in apoptosis and claim that “HIV” causes apoptosis—even if the particles (arrowed by them) in their “purified HIV” preparations are indeed a retrovirus “HIV”. Since their preparation contained so many impurities one cannot tell what causes the apoptosis.
References 1. Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, Causer D, Alphonso H, Miller T. (1999). A critical analysis of the pharmacology of AZT and its use in AIDS. Current Medical Research and Opinion 15:1s-45s. www.theperthgroup.com/SCIPAPERS/cmroazt.html 2. British HIV Association guidelines for anti-retroviral treatment of HIV seropositive individuals. (1997) Lancet, 349, 1086–1092. 3. Saag MS, Holodniy M, Kuritzkes DR, O’Brien WA, Coombs R, Poscher ME, Jacobsen DM, Shaw GM, Richman DD, Volberding PA. (1996). HIV viral load markers in clinical practice. Nat. Med., 2, 625–629. 4. Papadopulos-Eleopopulos E, Turner VF, Papadimitriou JM, Hedland-Thomas B, Causer D, Page B. (1995). A critical analysis of the HIV-T4-cell-AIDS hypothesis. Genetica 95:5-24. www.theperthgroup.com/SCIPAPERS/ept4cells.html 5. Piedimonte G, Guetard D, Magnani M, Corsi D, Picerno I, Spataro P, Kramer L, Montroni M, Silvestri G, Torres Roca JF, Montagnier, L. (1997). Oxidative protein damage and degradation in lymphocytes from patients infected with human immunodeficiency virus. Journal of Infectious Diseases 176:655-64. Competing interests: None declared |
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Alexander H Russell, Philosopher/artist/writer WC1N 1PE
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Dr. Flegg has constantly failed my challenge to provide visual evidence for the existence of ‘HIV’ and offers yet more weak obfuscation by stating: “I suggest that if Russell spends some time reading previous responses in the BMJ debates on HIV he may find the information he seeks. His antiquated definitions of what constitute viral identification and isolation do not apply in current molecular virology.” Anyone who has studied the developments in microbiology, and in virology/retrovirology in particular, during the last 30 years will have observed a shift in emphasis from strictly applied rules of empirical observation, the backbone of true scientific method, to a sloppy form of virtual virology, reliant on assumptions based more on a sort of gnostic wishful thinking rather than provable scientific fact. The rot began to set in during the mid-70’s when Robert Gallo was trying to prove that a retrovirus, HTLV1, was the cause of a novel form of leukaemia – adult T-cell leukaemia*. During his studies of HTLV1, Gallo admits to having been puzzled by his failure to observe any viral particles in the infected blood and tissues. However, he decided one did not need to be able to see a virus, but could infer its presence from surrogate markers – antibodies specific to supposed viral proteins, chemical markers etc. By then, microbiologists were abandoning electronmicroscopic evidence of viral infection as being too time- consuming to carry out, and out-dated. For reasons best known to themselves our contemporary crop of virtual virologists claim that it is not necessary to be able to see densely packed ‘HIV’ particles to prove that they exist. The reason they say this is because they know very well they cannot see any ‘HIV’ because there is none to see. Since human retroviruses could never be seen in supposedly infected tissues using well tried and trusted traditional visualisation techniques (EM), the failed anti-cancer careerists who switched gravy trains to the more lucrative study of ‘AIDS’, resorted to sharp-practice and moved the goal-posts in order to keep their laboratories open and funded. It is my contention, however, that they dare not trust ‘old- fashioned’ methods of confirming the virus’ existence because no ‘HIV’ will be seen. ‘HIV’ must be seen to be active and replicating at high titre for them to claim it is causing ‘AIDS’. Even a ‘retrovirus’ must obey the basic law of physics – it has to do something to cause something to happen. In 20 years, ‘HIV’ has never been observed at a pathologically significant titre in a single case of supposed infection. Subsequently this has led to all sorts of anomalies in retrovirology, and the study of the putative ‘HIV’ in particular. The Perth Group have outlined these anomalies in exhaustive detail elsewhere. If Dr. Flegg is right then surely there is no harm in using what he considers to be old-fashioned methodology (“antiquated definitions of what constitute viral identification”) to show that HIV exists. That would have the twofold effect of convincing sceptics like myself of the truth of HIV’s existence, and confirming that their new methods of viral identification are indeed valid. *Of course, thanks to Duesberg, we now know that this cannot be so for two principal reasons. a. A randomly integrating retroviral genome, as HTLV1 is supposed to be, capable of turning an infected cell cancerous, would result in polyclonal cancers. Such cancers have never been observed in vivo, all naturally occurring cancers being monoclonal. b. There is still no evidence that cancer is a transmissible infectious disease, although the human papiloma virus has its supporters as an infectious, cancer-causing agent. Competing interests: None declared |
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Eleni Papadopulos-Eleopulos, Biophyicist 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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Regarding the Continuum Reward
In his rapid response “Response to Russell: even Duesberg has “proved HIV existence””, 15th April 2004, Peter Flegg wrote: “…I have yet to see a coherent response to Duesberg from the dissident lobby.”
Peter Duesberg was and remains a highly regarded opponent of the “HIV” theory of AIDS. A response to Peter’s claim of proof of “HIV” isolation was published in Continuum (Continuum Vol 4, No. 3. Sept/Oct 1996) under the title “The Isolation of HIV – Has It Really Been Achieved? The Case Against” and can be found at www.theperthgroup.com/CONTINUUM/pgvsduesbergreward.html
Competing interests: None declared |
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Simon Portsmouth, Consultant St Marys Hospital W2 1NY
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I am glad many of the dissidents are distracted by the debates on these pages and not trying to influence those who can benefit from the enourmous advantages of treatment for HIV. In our HIV clinics we have been able to dramatically alter our patients lives from those of misery and despair to hope and freedom from suffering. Before combination antiretroviral treatment we could only give comfort and pain relief and watch our brave patients die. I don't need to enter the argument you have been having - I have patients to see who are very grateful for the life we can now offer them. Competing interests: I find it rewarding to reverse the illness death and misery of my patients by succesffully treating their HIV with drugs that they tolerate very well and with minimal toxicity. |
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Peter Flegg, Consultant Physician Blackpool UK, FY3 8NR
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Professor Duesberg has provided evidence for HIV's existence. I did indeed state that “I have yet to see a coherent response to Duesberg from the dissident lobby.” I thank the Perth Group for alerting eBMJ readers to their response to Duesberg's claims (3rd May). Nonetheless, my original statement still stands. Competing interests: None declared |
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Eleni Papadopulos-Eleopulos, Biophysicist 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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One More Question to Peter Flegg In his rapid response, “Re: Re: Response to Russell: even Duesberg has “proved HIV existence””, 4th May 2004, Peter Flegg wrote: “Professor Duesberg has provided evidence for HIV's existence. I did indeed state that “I have yet to see a coherent response to Duesberg from the dissident lobby.” I thank the Perth Group for alerting eBMJ readers to their response to Duesberg's claims (3rd May). Nonetheless, my original statement still stands.” Would please Peter Flegg tell us whether his “original statement still stands” because he hasn’t read our response to Peter Duesberg’s claims? Competing interests: None declared |
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Alexander H Russell, Philosopher/artist/writer WC1N 1PE
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Dr. Peter Flegg stated: "Professor Duesberg has provided evidence for HIV's existence." But where is Duesberg's visual evidence that proves 'HIV' exists? BMJ readers may be pondering why Dr. Flegg obfuscates and fudges all the time by making absurd references to worthless 'HIV' virtual virology papers. I have a new word for Flegg's obfuscation for the Oxford English Dictionary: Flegging. Flegging is when one fails to answer directly and takes people on detours to avoid questions and avoid answers. Dr. Flegg will not give BMJ readers the visual evidence that 'HIV' exists but will go on and on and on Flegging! I ask yet again: can Dr. Flegg show me visual evidence; i.e. in a published electronmicrograph, of massed, densely packed purified 'HIV' particles (isolated from all other contaminants) found in a fresh blood sample? BMJ readers must be informed that in 20 years of over-funded 'HIV' pseudoscience no one has ever done this. Why? I ask Dr.Flegg yet once again: prove that 'HIV' exists via visual EM evidence. And this time: just purified 'HIV' devoid of cellular debris and microvesicles. The isolated 'HIVs' should be intact, enveloped retroviruses which should be easily visible! EM evidence for 'HIV' retroviral particles is still missing! Competing interests: None declared |
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Peter Flegg, Consultant Physician Blackpool UK FY3 8NR
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I see Russell has invented a neologism, "Flegging", to describe the process of providing evidence by studying the contents of scientific research papers. I am delighted by this accolade, and hope his suggestion will be taken up and gain general acceptance forthwith. I fail to see how pointing Russell to published research is "obfuscation" or fudging". How does Russell conclude all these papers I have cited are "worthless" - does a philosopher/artist/writer know more virology than the publishing editors and peer reviewers of the leading science journals? Turning to what I think is the point of Russell's e-letter, I have never claimed Duesberg provided visual proof for HIV. I pointed out that if, in his capacity as one of the world's pre-eminent retrovirologists, he was satisfied there was sufficient molecular-biological evidence for the existence of HIV, then that should be good enough for most people. I have not provided Russell with references to electron micrographs for HIV. These were provided by Brian Foley on 6th May (Re Re Re Two questions to Brian Foley). Perhaps Russell will just have to overcome his distaste and read those nasty "worthless 'HIV' virtual virology papers" after all. Competing interests: None declared |
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Peter Flegg, Consultant physician Blackpool UK FY3 8NR
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The Perth Group claimed that there is no evidence that HIV is responsible for T4 lymphocyte depletion. Their precise words were: “Although no effort has been spared, nobody (has) been able to present evidence which proves that “HIV” kills the T4 cells either directly or indirectly by apoptosis or by any other mechanism.” The reference for this claim is a paper the Perth Group authored some years ago and which is to be found on their web site, and which they say contains evidence supporting their view.
The topic of lymphocyte depletion has been an intensely active one for biomedical research, not least because of its great therapeutic potential. We know HIV induces CD4 depletion and that apoptosis plays a crucial part. In addition to the articles I recommended to the Perth Group, I suggest they read some other more recent reviews and articles (1-5). It may be perfectly true that some scientists question the significance of apoptosis, but even then they do not dispute that HIV induces CD4 depletion.
Current research usually does not focus on whether apoptosis occurs, but why and how. Apoptosis in uninfected cells can be induced in several ways, both through caspase-dependent activation through Fas-mediated activation-induced cell death or HIV accessory proteins inducing uninfected bystander cell death and through caspase-independent pathways. I am not a molecular immunologist and cannot pretend to understand all the details involved, but a glance at some of the publications referenced below will give readers a clue as to the nature of ongoing work in apoptosis.
If one looks more closely at the arguments the Perth Group deploys to deny the existence of apoptosis, their weaknesses become readily apparent. A few of their main points can be summarised as follows:
1. HIV pioneers like Gallo and Montagnier were unsure 20 years ago what caused lymphocyte depletion. (Comment: a lot has changed since – I rather think they have a better idea now).
2. Thirteen years ago the researchers who hypothesised apoptosis as a mechanism for T cell death suggested a mechanism for it that some later researchers did not corroborate (Comment: These researchers still confirmed that apoptosis occurred, even if they disputed the mechanism).
3. In 1991 Luc Montagnier did an experiment with CEM cultures and showed that following HIV infection maximal apoptosis preceded maximal viral production. (Comment: This hardly indicates the processes are independent. It is a bit like saying Johnny ate all the pies for lunch even though he wasn’t as hungry then as he would have been at teatime).
4. Montagnier proposed oxidative stress as a mechanism for apoptosis (Comments: the word “proposed” is specifically emphasised by the Perth Group, but I would have thought they would be the first to point out a proposal does not equal proof. Oxidative stress can be induced by HIV infection).
5. Researchers talk about the “apoptosis hypothesis” when discussing the pathogenesis of T cell depletion (Comment: Perhaps, like Montagnier, they should have used the term “proposal” rather than “hypothesis” in order for the Perth group to believe them).
6. Even where apoptosis has been shown to occur, “contaminants” or other factors are hypothesised, er sorry, are proposed to be responsible, and not HIV itself (Comment: at least the Perth Group accepts that apoptosis does occur concurrent with HIV infection).
The Perth Group go on to reveal their true colours by defining their own quirky scientific rules for proof of HIV-apoptosis, in a somewhat similar fashion to the genesis of their own rules for “proof of virus isolation”, or “proof for sexual transmission”. They say the only way to prove HIV causes apoptosis is to demonstrate that “the introduction of purified “HIV” in cell cultures or when administered to animals leads to a significant increase in apoptosis as compared to the appropriate controls”. On the face of it, reasonable enough one might think, but the statement contains their usual get-out clause. The Perth Group do not believe in the concept of “purified HIV” without “contamination”, so they rest secure in the knowledge that despite thousands of papers on the subject, no one could ever prove that HIV causes apoptosis (or for that matter anything at all) to their satisfaction.
Nevertheless, several studies would actually meet their criteria. These include studies using “infectious molecular clones” of HIV or SHIV. One of these demonstrated profound apoptosis occurring in macaques infected with an SHIV(DH12R) chimera(6). In another (7), different strains of SHIV(89.6p and NM-3rN) both induced apoptosis, the latter only at high concentrations (despite presumably equivalent “impurities” being present at the lower concentrations where 89.6p induced apoptosis but the non-pathogenic NM-3rN did not). In one study researchers used molecular clones of Env gene HIV-1 mutants to induce apoptosis in order to study the Env/CD4 signalling processes in vitro (8). Apoptosis has also been shown to occur in rodents transgenic for HIV accessory proteins (9,10).
It would also be interesting to see how the Perth Group explains away apoptosis that occurs with other viral/retroviral infections (11,12), even other CD-4 tropic immunodeficiency-retroviruses (13). Does the Perth Group dispute the existence of apoptosis-inducing retroviruses like SIV (14), or is it only HIV that is mythical? Why does apoptosis occur in animals and humans in vivo without the added “contamination” of mitogens or mycoplasmas? Why is productive infection with certain pathogenic HIV strains (X4) associated with apoptosis, but not with less pathogenic (R5) strains and inactivated virions (despite the “apoptosis-inducing contamination” of these “impure” viruses being equivalent)(15)?
In such a large research field, it is not hard to come up with some scientific papers that will appear contradictory, and apoptosis is no exception. What is required is a little objectivity in assessing their contribution to the overall understanding of the topic. The practice of “quote-mining” as carried out by many dissidents in an attempt to find “evidence” supporting their biased view does little to advance the scientific understanding of a difficult subject.
References.
(1) J. B. Alimonti, T. B. Ball, and K. R. Fowke. Mechanisms of CD4+ T lymphocyte cell death in human immunodeficiency virus infection and AIDS. J. Gen. Virol 2003; 84(7): 1649–1661.
(2) Selliah N, Shackelford J, Wang JF, Traynor F, Yin J, Finkel TH. T cell signalling and apoptosis in HIV disease. Immunol Res. 2003; 27(2-3):247-60.
(3) Grossman Z, Meier-Schellersheim M, Sousa AE, Victorino RM, Paul WE.
CD4+ T-cell depletion in HIV infection: are we closer to understanding the cause?
Nat Med. 2002; 4:319-23.
(4) Douek DC. Disrupting T-cell homeostasis: how HIV-1 infection causes disease. AIDS Rev. 2003 Jul-Sep;5(3):172-7.
(5) Ross TM. Using death to one's advantage: HIV modulation of apoptosis.
Leukemia. 2001; 15(3):332-41.
(6) Igarashi T, Brown CR, Byrum RA, Nishimura Y, Endo Y, Plishka RJ, Buckler C, Buckler-White A, Miller G, Hirsch VM, Martin MA. Rapid and irreversible CD4+ T-cell depletion induced by the highly pathogenic simian/human immunodeficiency virus SHIV(DH12R) is systemic and synchronous. J Virol. 2002;76(1):379-91.
(7) Iida T, Kita M, Kuwata T, Miura T, Ibuki K, Ui M, Hayami M, Imanishi J.
Apoptosis induced by in vitro infection with simian-human immunodeficiency chimeric virus in macaque and human peripheral blood mononuclear cells. AIDS Res Hum Retroviruses. 2001 Oct 10;17(15):1387-93.
(8) Holm GH, Zhang C, Gorry PR, Peden K, Schols D, De Clercq E, Gabuzda E. Apoptosis of Bystander T Cells Induced by Human Immunodeficiency Virus Type 1 with Increased Envelope/Receptor Affinity and Coreceptor Binding Site Exposure. Journal of Virology, 2004: 78:9 4541-4551.
(9) Yasuda J, Miyao T, Kamata M, Aida Y, Iwakura Y. T cell apoptosis causes peripheral T cell depletion in mice transgenic for the HIV-1 vpr gene. Virology. 2001 Jul 5;285(2):181-92.
(10) Reid W, Abdelwahab S, Sadowska M, Huso D, Neal A, Ahearn A, Bryant J, Gallo RC, Lewis GK, Reitz M. HIV-1 transgenic rats develop T cell abnormalities. Virology 2001;285(2):181-92.
(11) Bitzer M, Prinz F, Bauer M, Spiegel M, Neubert WJ, Gregor M, Schulze-Osthoff K, Lauer U. Sendai virus infection induces apoptosis through activation of caspase-8 (FLICE) and caspase-3 (CPP32). J. Virol. 1999; 73:702-708.
(12) Bonzon C,Fan H. Moloney murine leukemia virus-induced preleukemic thymic atrophy and enhanced thymocyte apoptosis correlate with disease pathogenicity. J. Virol 1999; 73:2434-2441.
(13) K Saha, P H Yuen, and P K Wong. Murine retrovirus-induced depletion of T cells is mediated through activation-induced death by apoptosis. J Virol. 1994; 68 (4): 2735–2740.
(14) Monceaux V, Estaquier J, Fevrier M, Cumont MC, Riviere Y, Aubertin AM, Ameisen JC, Hurtrel B. Extensive apoptosis in lymphoid organs during primary SIV infection predicts rapid progression towards AIDS. AIDS. 2003 Jul 25;17(11):1585-96.
(15) Sylwester AW, Grivel J-C, Fitzgerald W, Rossio JL, Lifson JD, Margolis LB. CD4+ T-Lymphocyte Depletion in Human Lymphoid Tissue Ex Vivo Is Not Induced by Noninfectious Human Immunodeficiency Virus Type 1 Virions. J Virol 1998: 72, 11: 9345-9347.
References on mechanisms of HIV-apoptosis:
Chen D, Wang M, Zhou S, Zhou Q. HIV-1 Tat targets microtubules to induce apoptosis, a process promoted by the pro-apoptotic Bcl-2 relative Bim. EMBO J. 2002 Dec 16;21(24):6801-10.
Silvestris F, Grinello D, Del Prete A, Cafforio P, Quarto M, Dammacco F. Anti-Fas (CD95/Apo-I) autoantibodies and soluble Fas levels concur in T cell depletion in HIV type 1 infection. AIDS Res Hum Retroviruses. 2001 May 1;17(7):603-14
Jekle A, KepplerOT, De Clercq E, Schols D, Weinstein M, Goldsmith MA. In Vivo Evolution of Human Immunodeficiency Virus Type 1 toward Increased Pathogenicity through CXCR4-Mediated Killing of Uninfected CD4 T Cells. J. Virol 2003; 5846-5854, Vol. 77, No. 10
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Competing interests: None declared |
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Alexander H Russell, Philosopher/artist/writer WC1N 1PE
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"I see Russell has invented a neologism, "Flegging", to describe the process of providing evidence by studying the contents of scientific research papers. I am delighted by this accolade, and hope his suggestion will be taken up and gain general acceptance forthwith." Flegging means obfuscation and prevarication since Flegg has never provided: " …evidence by studying the contents of scientific research papers " for proof of the existence of ‘HIV’ but merely flegged i.e. reiterated flawed and fraudulent 'HIV' virtual virology research and naively, gullibly and uncritically believed in all this nonsensical ‘HIV’ pseudoscience. Flegg states: "How does Russell conclude all these papers I have cited are ‘worthless’ - does a philosopher/artist/writer know more virology than the publishing editors and peer reviewers of the leading science journals? " Yes! Absolutely! Because they are all blindly labouring under a complete misapprehension: so-called ‘HIV’ has become yet another mythical ‘weapon of mass destruction’ that no one has proved ever existed! Nearly 200,000 papers, all based on a mistaken belief that a unique retrovirus, ‘HIV’, has been isolated, are all completely worthless. The taxonomy of 'HIV' was due to a pre-emptive political move to convince a worried world they had found the cause of 'AIDS'. Nature, Science, The Lancet, New Scientist, Scientific American and the New England Journal of Medicine have all been propagating the global ‘HIV’ fraud and simply cannot admit at this late stage that they all got it tragically and blindly wrong. These journals dare not admit that ‘HIV’ simply does not exist: their reputations are tied to the promotion of highly profitable ‘HIV’ propaganda.. Remember that scurvy, beri beri, and pellagra were all originally treated as infectious diseases rather than vitamin deficiencies: how many doctors provided completely inappropriate treatment for their patients based upon the received wisdom? 'AIDS' has also been treated as an infectious condition when it clearly is not. More recently, the outbreak of smon in Japan, a disease which caused mass paralysis and blindness, was attributed to a virus named the Inoui Virus; subsequent research carried out against strong opposition from the powers that be proved that the disease was caused by massive over prescription of the drug Clioquinol marketed in Britain as Enterovioform to treat diarrhoea. Think Dr. Flegg: have you ever prescribed Enterovioform? How would you have treated pellagra in the 1920's? Had you been a ship’s doctor in the 18th century, would you have sanctioned the throwing overboard of patients suffering from scurvy? Those doctors were wrong but were only acting on received wisdom, which let them and their patients down. Now ‘AIDS’ doctors are doing exactly the same thing: prescribing inappropriately dubbed ‘antiviral’ drugs for a hypothetical ‘retrovirus’ (‘HIV’) that does not exist? Plus ca change... Alexander H Russell Competing interests: None declared |
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Peter J Flegg, Consultant physician Blackpool, UK FY3 8NR
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I thank Alexander Russell for revealing so clearly the true evidence base for his viewpoint. Perhaps the new word of the week should be "Russelling". At the moment I am not sure whether to define this as: "Packing a single sentence with as many innapropriate and irrelevant expressions one can possibly think of", or alternatively a term indicating unflinching belief in the global scientific conspiracy of HIV, or merely another term for the effect of cognitive dissonance. Competing interests: None declared |
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Bob Bury, Consultant Radiologist Leeds General Infirmary LS1 3EX
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I am struck by the similarities between this discussion and that on Munchausen syndrome by proxy (MSBP). In both cases the protagonists advance their case with religious fervour, and it is quite clear that scientific argument is never going to have any influence on their opinions. Mr Russell is a philosopher/writer/artist, so you wouldn't go to him for treatment of your HIV-related illness. You might, however, expect him to know a bit about the rules governing logical argument. And yet we see him using the fact that doctors were once wrong about the causes of beri- beri as having some kind of relevance to his belief that they are now wrong about HIV and AIDS. As someone who actually treats AIDS patients made clear above, the AIDS/HIV model is at the very least a valid working hypothesis, given that it has led to advances in treatment, whereas the results of Mr Mbeki's evangelical opposition to the hypothesis are only too clear to see in South Africa. I sometimes wonder what the refuseniks in these situations get out of their crusading opposition to the weight of scientific evidence, since there must presumably be something in it for them. I suspect a decent philosopher might be able to help us with that. Anybody know one? Competing interests: None declared |
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