Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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Re: Withdrawal of Generic (Antiretroviral Drugs) ARVs by Ranbaxy
- Musa Garbati (21 November 2004)
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Do cheap Antibiotics halve AIDS deaths?
- Alexander H Russell (23 November 2004)
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Re: Do cheap Antibiotics halve AIDS deaths?
- Nicholas Bennett (24 November 2004)
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Re: Do cheap Antibiotics halve AIDS deaths?
- Trevor G Marshall (24 November 2004)
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Reply to Nicholas Bennett: 'HIV' & lymph nodes
- Alexander H Russell (25 November 2004)
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Re: Do cheap Antibiotics halve AIDS deaths?
- John P Heptonstall (26 November 2004)
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Re: Reply to Nicholas Bennett: 'HIV' & lymph nodes
- Nicholas Bennett (26 November 2004)
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Reply to Nicholas Bennett: what does 'HIV' look like?
- Alexander H Russell (27 November 2004)
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Re: Reply to Nicholas Bennett: what does 'HIV' look like?
- Nicholas Bennett (28 November 2004)
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Reply to Bennett: True isolation of 'HIV' from a fresh blood sample has never been achieved.
- Alexander H Russell (3 December 2004)
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Re: Reply to Bennett: True isolation of 'HIV' from a fresh blood sample has never been achieved.
- Nicholas Bennett (4 December 2004)
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Reply to Bennett: EM is essential to confirm that 'HIV' exists
- Alexander H Russell (7 December 2004)
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Musa Garbati, Consultant Physician University of Maiduguri Teaching Hospital, P.M.B. 1414, Maiduguri, Nigeria
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I read the disturbing development on the above subject matter which I find very disturbing indeed. This is happening barely five months after the withdrawal of two other generic (Acquired immune Deficiency Syndrome)AIDS drugs in June this year, for the same reason.1 This brings the list of withdrawn ARVs to eight since June 2004. The generic antiretroviral agents in question have been said not to have the desired bioequivalence although the drugs have been the most widely used ARVs in most developing countries. Practitioners in many third world countries can attest to this. Before the introduction of generics to these countries management of HIV/AIDS and related conditions have been limited to just treatment of opportunistic infections (OIs). The other available ARVs in at least the Nigerian markets were either difficult to come by or out of reach of the poor. For the HIV infected (and affected) in the developing world like Nigeria, with an average seroprevalence rate of 5.8%,2 the coming of generic ARVs was seen as the best thing that has ever happened to persons living with HIV/AIDS (PLWAs) towards the alleviation of their sufferings. Generics produced by Ranbaxy and Cipla are the most popular ARVs in many Nigeria markets (and other developing countries). The introduction of one of the products, Triomune, a three in one pill combining lamivudine, stavudine, and nevirapine, has been of particular relief to a lot of our patients due to improved compliance. For a pandemic that is spreading around the world, infecting more than 14,000 individuals per day,3 this move by WHO if not followed by the provision of alternative ARVs is likely to be the disaster of the year. Alternatives should not just be made available but affordable to those that need it most. These drugs are withdrawn not because they are unsafe or of poor quality, but because they may not be as effective as they should be. Since the problem now is of bioequivalence I would like a situation where by WHO and its sister agencies to as a matter of urgency make alternative arrangements to making branded ARVs available to the developing world. If not the current success that we are beginning to record as far as the management of HIV/AIDS is concerned will be just be a thing of the past, in a matter of months. From the words of Peter Graaff from WHO’s AIDS medicines and diagnostics service,1 that WHO was just advising countries to suspend the use of these drugs but for those that do not have alternatives, continued use should be weighed against the risks of interrupting treatment. References 1. Fiona Fleck. WHO pulls three more AIDS drugs from list. BMJ 2004; 329: 368. 2.Gwarzo S, Eloike T, Ekanem EE, Elong O, Gboun F. The 2001 National HIV/Syphilis Sentinel Survey among pregnant women attending ANC in Nigeria. FMOH, Nigeria. 2001. 1:51 3. Schenker II, Nyirenda JM. Preventing HIV in schools. Educational and practices series. 2002; 9:6 Dr Musa A. Garbati Consultant Physician University of Maiduguri teaching Hospital, Maiduguri, Nigeria E-Mail: musagarbati@yahoo.com Competing interests: None declared |
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Alexander H Russell, Writer/artist/philosopher WC1N 1PE
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Dr Musa A. Garbati alarmingly stated: "For a pandemic that is spreading around the world, infecting more than 14,000 individuals per day,3 this move by WHO if not followed by the provision of alternative ARVs is likely to be the disaster of the year. Alternatives should not just be made available but affordable to those that need it most." What evidence does Dr. Garbati have for these fictitious figures of "14,000 individuals per day" being 'infected' with 'HIV'? Even the 'AIDS' establishment admit - and are agreed - that 'HIV' is very difficult to 'transmit'. These wildly inflated figures are abstract and arbitrary and are all based on 'guesstimates' which in the past have invariably been wrong. How many of these alleged "14,000" individuals have had a 'positive' ELISA 'HIV' test, confirmed by Western Blotting, and further confirmed by the recovery of a significant quantity of viable infectious 'HIV' particles from said patient? The answer may surprise Dr. Garbati: zero. What studies have ever been carried out to recover 'HIV' particles from the blood of these individuals? The answer is none. If "14,000 individuals" are being 'infected' by 'HIV' daily then where is the 'HIV' epidemic in the West? Where are all the 100,000s of Western heterosexuals with 'HIV' or 'AIDS'? There is no heterosexual 'HIV' epidemic in the West (or anywhere else in the world for that matter). Does Dr Garbati realise that TB, malaria and disease conditions relating to poverty in the developing world make these non-standardised and non- specific arbitrary 'HIV' tests run 'positive'? What we are wrongly calling 'HIV' is merely an endogenous marker for 'risk-behaviour' in the West and disease-conditions relating to poverty and malnutrition in the developing world. So-called 'anti-retroviral' drugs cannot cure 'AIDS' related conditions such as TB and malaria. All 'anti-retroviral' drugs can do is interfere with the bodies natural metabolism and make matters worse. There is no such thing as an 'anti- retroviral' drug anyway because 'HIV' is really an endogenous epiphenomenon. What poor Africans really need is clean water, sanitation, nourishing food and not over priced and highly toxic 'antiretrovirals'. All endemic diseases of Africa are made infinitely worse by malnutrition: their bodies do not have the basis resources to fight disease. The last things poor Africans need is expensive and lethal 'anti-retroviral' drugs. We now see Septrin is being touted as the great, low-cost saviour antibiotic for 'AIDS' related illnesses in African children, halving the death rates previously attributed to the hypothetical 'HIV' infection. We are told that co-trimoxazole has the advantage of being cheap and readily available, whereas 'anti-retroviral' drugs are much more expensive. Co- trimoxazole costs less than ten cents per person a day. It is well known that antibiotics are powerless against viruses – including 'retroviruses' - so if the patients are recovering when put on Septrin this must be because Septrin is active against bacterial infections. However, if it is claimed that 'X' million children a year die of malaria with or without 'HIV' then the malaria is obviously the main problem and 'HIV' is irrelevant. If Septrin is halving 'AIDS' deaths then obviously their 'HIV' status is irrelevant; antibiotics have no effect on viruses, retro or otherwise. What the Septrin is killing is the mycoplasmas which are the true cause of cell death. This was shown to be the case by Luc Montagnier himself in a series of experiments. Montagnier showed when 'HIV' infected cell cultures were dying, adding doxycyclin to those cultures, the cells no longer died and continued to replicate 'HIV' with no apparent damage. Apparently the antibiotic he used destroyed a highly hypoxic mycoplasma which he called mycoplasma neoformans or mycoplasma incognitus. We can only eradicate 'AIDS' in the developing world by removing 'HIV' from the equation and abolishing lethal 'anti-retroviral' drugs. We have been 'informed by WHO that there are 12 million (so-called) 'AIDS' orphans in Africa - and a million have 'HIV'. Such white Western fantasies can fuel racist attitudes and images about Africans being 'sexual savages' spreading 'AIDS' like wild fire. We need to stop using the racist slogan 'AIDS' and start to treat people for the actual (rather than virtual) disease-conditions that they may have. I ask Dr. Garbati to consider my points with an open mind. References: 'Antibiotic halves HIV/Aids deaths', BBC News UK Edition: Friday, 19 November 2004. Competing interests: None declared |
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Nicholas Bennett, Infectious Disease Postdoc/Clinician Department of Pediatrics, University Hospital, Syracuse NY
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Dear Editor, The mycoplasma story is a classic among those claiming that HIV is harmless. A very little research shows that the cell line in question (CEM) was a mixed lineage line, containing CD4+ and CD4- cells. In the prescence of HIV all the CD4+ cells died, but the CD4- cells grew to replace them [1]. When co-infected with the mycoplasma, CD4+ and CD4- cells died non-selectively. The use of antibiotics in this case, coupled with proper analysis of the cell line, actually proves that HIV neatly kills CD4+ cells in vitro. This story also highlights the dangers of reading the literature without knowing enough about the field. On a more practical note, the use of antibiotics in preventing AIDS deaths is rather obvious: since HIV doesn't kill people, but the secondary infections due to the immune suppression of AIDS will kill. This is why in serious infections the antivirals may be temporarily stopped to prevent poly-pharmacy side effects, and why prophylactic antibiotics are regularly administered to people with progressive HIV infection: and heart valves, cystic fibrosis, antibody deficiencies, neutropenia... If HIV is a harmless endogenous phenomenon and the drugs are toxic, can Mr Russell explain the fact that HIV seropositivity (i.e. infection) produces disruption of lymph node architecture [2], that is restored, along with CD4 T cells, once antiretrovirals are administered [3]? Can he explain why withdrawal of the drugs results in the reappearance of lymph node damage and a drop in CD4 T helper cells? [4] Nick Bennett njb35@cantab.net ref: 1. Yelle et al Arch Virol 1994;139(1-2):155-72 "Analysis of long- term viral expression in CEM cells persistently infected with non syncytium-inducing HIV-1 strains." 2. Zhang et al. Proc Natl Acad Sci U S A 1999, 96:5169±5172. "Reversibility of the pathological changes in the follicular dendritic cell network with treatment of HIV-1 infection. 3. Orenstein JM et al. AIDS 1999, 13:2219±2229. "Lymph node architecture preceding and following 6 months of potent antiviral therapy: follicular hyperplasia persists in parallel with p24 antigen. Restoration after involution and CD4 cell depletion in an AIDS patient. 4. Orenstein et al AIDS. 2000 Aug 18;14(12):1709-15. "Rapid activation of lymph nodes and mononuclear cell HIV expression upon interrupting highly active antiretroviral therapy in patients after prolonged viral suppression." Competing interests: None declared |
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Trevor G Marshall, Director Autoimmunity Research Foundation, California 91360
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Dr Russell said "Montagnier showed when 'HIV' infected cell cultures were dying, adding doxycyclin to those cultures, the cells no longer died and continued to replicate 'HIV' with no apparent damage" Has this work of Montagnier been published? I did find "Mycoplasmas as cofactors in infection due to the human immunodeficiency virus" (PMID: 8399934) but that doesn't seem to cover this Doxycycline experiment. Is a citation available that describes this study in more detail? Competing interests: None declared |
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Alexander H Russell, Writer/artist/philosopher WC1N 1PE
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Nicholas Bennett stated: If HIV is a harmless endogenous phenomenon and the drugs are toxic, can Mr Russell explain the fact that HIV seropositivity (i.e. infection) produces disruption of lymph node architecture." How do we know that the particles are 'HIV and how do we know it is 'HIV' that is disrupting the lymph nodes? What else is in there? If 'HIV' is sequestered in the lymph nodes, as claimed, how can it be actively damaging the immune system? There are cases recorded in the literature of people who have never tested 'HIV' positive who nevertheless have swollen lymph nodes. On examination, the nodes are shown to contain particles morphologically identical to 'HIV'. However there is no evidence that these particles are destroying the lymph nodes, merely that they are being sequestered there. On examination the tissues were shown to contain morphologically identical particles to 'HIV'. Hoe does Mr. Bennett explain that morphologically identical particles to 'HIV' can be found in virtually all placental tissue examined under electronmicroscopy? What is "HIV seropositivity (i.e. infection"? There is still no evidence that 'HIV' is an 'infectious' agent; it is only assumed to be. Competing interests: None declared |
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John P Heptonstall, Director of the Morley Acupuncture Clinic Leeds LS27 8EG
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Sir Although I agree with the thrust of Alexander Russell's arguments I would point out that Septrin was effectively 'banned' in the UK some years ago - other than for infections other drugs could not affect - after having been cited as unsafe, especially for children. It was also suggested that trimethoprim (part of the trimethprim/ sulphonamide mix which is co-trimoxazole or Septrin) was equally as effective as Septrin at dealing with infections -the Sulphonamide almost irrelevant. Jornalist Brian Deer wrote an excellent (and perhaps controversial) article at that time in the Sunday Times about the problems of the drug as a kind of expose, and of it's producer Wellcome. One wonders what problems so-called HIV+ve African kids are having from Septrin that go unannounced? Doxycycline, although not without potential ADRs, might be the better option. Regards John H. Competing interests: None declared |
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Nicholas Bennett, Infectious Disease Postdoc/Clinician Department of Pediatrics, University Hospital, Syracuse NY
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Mr Russell poses some concrete questions that I'm only too happy to answer, since I hope that by doing so he might appreciate more of where I'm coming from. "What else is in there?" is a very good question, since of course we're largely limited to observing what we know to look for (especially as regards the molecular techniques). We know the particles are HIV because, by the standards of distinguishing any other pathogen, they appear to be HIV. They have the morphology, genetic material and protein content of HIV. Mr Russell refers to several reports (previously quoted here) of EM photographs showing virus-like particles in some lymph node specimens. I have to say that I have yet to see a report where the particles are obviously indistiguishable from those of HIV - unless you ignore data in the paper. Either the morphology is _not_ the same as HIV, or molecular techniques show that the particles do not contain HIV genetic material and protein. The giveaway is that the HIV-type material is only seen in cases isolated from HIV+ patients. This strongly suggests that the material is from an infection with the same agent that caused the serology to change. To most scientists and clinicians, the strength of the immune response and molecular techniques makes this a QED. The placental story is absolutely fascinating! An endogenous retrovirus called HERV-W is activated and expresses some of its retroviral genes. [1] The envelope gene is called Syncytin, and was initially discovered to be crucial to forming the syncitiotrophoblast later of the placenta. It was only later shown to be from an endogenous retrovirus. Additionally, the immunosuppressive effects of this virus (all retroviruses are immunosuppressive to a certain degree, via their envelope protein) may protect the foetus from rejection by the mother. After all, the foetus is nothing if not a non-tissue matched organ graft! The intriguing part is considering that a retrovirus infected some animal millions of years ago and is now directly involved in the formation of a key part of the mamallian placenta - would there be mammals without this retrovirus...? Is it only a homonid phenomenon? Needless to say, Syncytin and HERV-W have been sequenced and don't have homology to HIV. Hence the placental particles aren't HIV. It may be however why pregnancy is a small risk for a false-positive HIV test: antibodies to endogenous RVs are made, albeit at low levels. Maybe there is a cross-reaction going on. I think this is only for the ELISA though, not for the confirmatory tests. Mr Russell also asks: "If 'HIV' is sequestered in the lymph nodes, as claimed, how can it be actively damaging the immune system? " This is the best place to damage the immune system! 60-80% of lymphocytes are in the lymph nodes. Only 10-20% will be in the peripheral bloodstream, and most of the activated cells (those preferentially infected by HIV) will traffic to the lymph nodes. The initial CD4 "recovery" seen in the first week or two of antiviral therapy is in fact due to redistribution of cells rather than a true recovery. The cells were there, just not in the bloodstream to be measured. Lymph node cultures can culture HIV even if viral load in the blood is "undetectable", but only if you're HIV+. The other particles do indeed just seem to be sitting there: only those identifiable as HIV seem to be related to lymph node damage and CD4 T cell loss. The mechanism is likely to be a mixture of cell death, chronic inflammation and over-stimulation and a disrupted cytokine environment. All of these occur and are reversable with treatment, but it's not clear yet which is _most_ important. B cells in particular lose their normal maturation sites in the nodes, but then overproduce ineffective antibodies. The lymph nodes are also home to cell types that bind HIV and present its antigens without themselves being vunerable to being killed off (the follicular dendritic cells). It is these cells that collect HIV from the mucosal surfaces and drag it into the body, straight into the sites best suited for its replication. I would say that there is plenty of evidence that HIV is an infectious agent. The sero-epidemiology looks like an infectious agent, the agent is transmissible in the lab and in experimental animal models, and just genetically it looks like an infectious agent (i.e. a retrovirus with intact, functional genes). Other infectious agents show weaker correlations than HIV between serology, PCR and culture: so in my eyes HIV surpasses the criteria for making the assumption it is an infectious agent. Are there other RVs and HERVs? Quite possibly. I've seen some data implicating retrovirus-like proteins and gene sequences in disease from multiple sclerosis to prostate cancer. It's possible that a recombination event between one of these and an SIV strain led to HIV. Mice, after all, are almost 100% infected with exogenous viruses like the Friend agent referred to elsewhere, and have at least 70 known endogenous retroviruses as well. I see no reason why we shouldn't have our own collection of harmless retroviral parasites. But HIV is not one of them. Nick Bennett njb35@cantab.net 1. Mi et al Nature. 2000 Feb 17;403(6771):785-9. "Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis." Competing interests: None declared |
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Alexander H Russell, Writer/artist/philosopher WC1N 1PE
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Mr. Bennett stated that: "We know the particles are HIV because, by the standards of distinguishing any other pathogen, they appear to be HIV." This is a ridiculous, circular argument – we don’t even know what ‘HIV’ looks like because it has never been isolated. How does Mr. Bennett know what 'HIV' looks like? We have not yet established what 'HIV’ looks like. No one has ever seen 'HIV' – not even Mr. Bennett. Why has Mr. Bennett still not provided an EM (electronmicrograph) reference of isolated/purified 'HIV'? How does Mr. Bennett know the 'particle' he is looking at is a virus? Mr. Bennett cannot escape the fact that Robert Gallo and Luc Montagnier did not isolate a virus. There is still no evidence that 'HIV' is a virus. Mr. Bennett stated: "I would say that there is plenty of evidence that HIV is an infectious agent." Where is this evidence? 'HIV' is presumed to be an infectious agent based purely upon rather shaky epidemiological evidence. However, no one has described in scrupulous detail how 'HIV' is transmitted from one individual to another. For instance what is the precise mechanism by which the receptive partner (heterosexual female or homosexual male) infects the insertive partner. Why is it that 'HIV' appears to be unidirectional? For a pathogen to survive in nature and spread in an epidemic form it has to be bi-directional in its transmission. This does not appear to be the case with 'HIV'. It is seldom or never found in peripheral blood of infectees so therefore how is 'HIV' transmitted from one individual to another. Certainly there is no evidence that animal retroviruses are transmitted sexually so why do we make the assumption that 'HIV' is transmitted this way? Traditionally retroviruses are alleged to be transmitted from female to offspring either in the womb or during breast-feeding but there is no suggestion that animal retroviruses are transmitted in semen. Nobody knows what 'HIV' looks like. Can Mr. Bennett provide an EM of isolated 'HIV'? Competing interests: None declared |
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Nicholas Bennett, Infectious Disease Postdoc/Clinician Department of Pediatrics, University Hospital, Syracuse NY
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The problem with Mr Russell's argument, is that you do not have to isolate something to know what it looks like. One early paper (from 1988) shows several EM micrographs of HIV showing the characteristic "truncated cone" core that is not seen in normal retroviruses. [1] One has to ask why these pictures must be ignored. This was just the first paper I pulled up with a 5 minute PubMed search, and incidentally also demonstrates how relative levels of reverse transcriptase can be used to attribute source (viral or cellular). Also, how is the epidemiology shaky? It is clear that bidirectional transmission DOES occur, since seroconversion to and from male and female partners has been well documented. To say otherwise is to ignore the evidence. The transmission HAS been described in scrupulous detail: HIV in semen or vaginal fluids, or blood, is transfered to the mucosal surface of the other partner. Dendritic cells transport the HIV to the lymph nodes. HIV infected CD4+ macrophages and T cells, and the resulting immune stimulation recruits yet more CD4+ T cells to be infected. This is all in the literature (and in the previously maligned Field's Virology!). HIV is found in 100% of infectees, as I have repeatedly demonstrated here, unless one chooses to ignore the findings of PCR and culture - generally considered Gold Standards for detection of a pathogen... There is plenty of evidence that animal retroviruses are transmitted sexually (e.g. [2] which shows an EM of wild mouse ecotropic virus within a semen sample): and besides, how could a pathogen that has a 5% per annum mortality, in the West, survive through solely vertical transmission? (and more importantly, not be noticed before? Death rates in some African HIV+ cohorts are over 30% by year 1, compared to 5% in uninfected children). If retroviruses are not transmitted horizontally, perhaps people should stop vaccinating their cats against Feline Leukaemia Virus, which is also a retrovirus. Paper [2] incidentally clearly demonstrates preferential male-to-female transmission, again at odds with what is expected of HIV. The words used by Mr Russell sounds strikingly like those of Duesberg in his original criticism of HIV's pathogenic role, but I hope that this evidence will help persuade Mr Russell that these statements were, in fact, entirely wrong. Additionally they should show that HIV, far from breaking any rules of virology, is in fact merely toeing the party line and behaving perfectly normally. Thirdly I hope that Mr Russell realises that some of what he believes to be true about retroviruses, and virology in general, is in fact not. I appreciate that he has the right to make informed decisions on a topic, even as an outsider, but experts are experts not just by token of working in a field, but through picking up the knowledge associated with it. Some other HIV EM's, to make the point that we really do know what it looks like. [4-6] Note that these papers used normal HIV EM as a _control_, since the field has moved on beyond trying to describe what HIV looks like. It's so much easier to simply state "HIV has no EM's" than to actually check out the facts. I wouldn't be surprised however if Mr Russell were not already aware of much of these images anyway, and therefore doesn't accept them. If that is the case, I would be interested in what _specific_ criticisms he has of their methodology - criticisms that cannot be applied to other areas of virology. Nick Bennett njb35@cantab.net 1. Gendelman et al J Exp Med. 1988 Apr 1;167(4):1428-41. "Efficient isolation and propagation of human immunodeficiency virus on recombinant colony-stimulating factor 1-treated monocytes." 2. Portis et al. J Virol. 1987 Apr;61(4):1037-44. "Horizontal transmission of murine retroviruses." 3. He et al. Science. 1984 Oct 26;226(4673):451-3. "HTLV-III in the semen and blood of a healthy homosexual man." 4. Welker et al. J Virol. 2000 Feb;74(3):1168-77. "Biochemical and structural analysis of isolated mature cores of human immunodeficiency virus type 1." 5. Ohagen et al J Virol. 2000 Dec;74(23):11055-66. "Role of Vif in stability of the human immunodeficiency virus type 1 core." 6. Shehu-Xhilaga et al J Virol. 2002 May;76(9):4331-40. "The conformation of the mature dimeric human immunodeficiency virus type 1 RNA genome requires packaging of pol protein." Competing interests: None declared |
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Alexander H Russell, Writer/artist/philosopher WC1N 1PE
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Mr. Nicholas Bennett stated: "The problem with Mr Russell's argument, is that you do not have to isolate something to know what it looks like." Mr. Bennett’s statement is ludicrous and an oxymoron and merely typifies the kind of sloppy science surrounding 'HIV' research. His statement is absolute nonsense: if the hypothetical 'HIV' has not been isolated how do we know what it looks like? I must remind Mr. Bennett that isolation means separating the target virus from all other contaminants. You have to establish which are viral proteins and which are contaminant proteins. No one has ever published EM images of isolated/purified 'HIV' recovered from a fresh blood sample or any other bodily fluid. Sloppy thinking and sheer laziness allowed scientists to get way with stating that material banding 1.16 in a sucrose density gradient represented 'pure retrovirus'. However, when this banded material was finally photographed under electronmicroscopy in 1997 it was revealed that practically all the banded material consisted of contaminants – microvescicles, cellular debris, etc., with just a few ambiguous dots which may or may not have represented the sought after hypothetical 'retrovirus'. It would be impossible from that mix when broken down into its constituent proteins to distinguish actual viral proteins from debris proteins. As for the point of knowing what something looks like, morphologically identical particles to those purporting to be 'HIV' can be found in the majority of placentas examined as well as in lymph node tissues biopsied from people with swollen lymph glands but with no indication of so-called 'HIV infection'. Luc Montagnier himself described the tissue cultures used in 'HIV' research as a "retroviral soup". When certain cell-lines are used it is possible using stimulants to activate previously latent endogenous retroviruses - yet another danger when making judgements based purely upon results obtained from cell culture. Mr. Bennett continues: "One early paper (from 1988) shows several EM micrographs of HIV showing the characteristic "truncated cone" core that is not seen in normal retroviruses." Please note: Mr. Bennett forgets to add that these particles are only ever observed in cell culture (in vitro)and have never been seen in this degree of clarity in any fresh blood or in any other bodily fluid. Laboratory conjuring tricks produce laboratory artefacts which should not be used for purposes of extrapolation. In a typical viral disease sufficient virus to cause the disease should be observable in the relevant tissues: this has never been the case for 'HIV'. Merely to say that the 'virus' is doing its lethal work from the comparative safety of the lymph nodes is a total cop out. Competing interests: None declared |
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Nicholas Bennett, Infectious Disease Postdoc/Clinician Department of Pediatrics, University Hospital, Syracuse, NY
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As an idea, I wonder if Mr Russell has considered the point that it's supremely easy to distinguish if the proteins in a soup are cellular of not. Look for them in the uninfected cells. Oddly enough, those alleged to be HIV are absent in uninfected cells by protein-based and (more importantly) genetic methods. There is really only one other conclusion: that they are viral. The concept can be taken to its limits by techniques such as subtractive hybridisation to detect upregulated or tissue-specific genes (pool x subtracted from pool y leaves only those genes or proteins unique to pool y). It's surprisingly easy to do - and needless to say has been done for HIV. Unless Mr Russell has some information from the human genome project that I am unaware of - i.e. that HIV genes have been detected, despite years of experiments showing the contrary. It is not so much laziness as using superior techniques (faster, cheaper, more accurate) which render others redundant: but I accept that it means that EM of peripherally isolated HIV will likely never be done - because it doesn't need to be done. This is NOT a unique situation to HIV science, contary to Mr Russell's assertations. If he looked elsewhere he would find it elsewhere. I'm still awaiting his acceptance that animal retroviruses can be horizontally transmitted, through sexual activity, and can additionally show preferential male-to-female transmission over female-to-male [1]. HIV (and the science behind it) is far from exceptional. Nick Bennett njb35@cantab.net 1. Portis et al. J Virol. 1987 Apr;61(4):1037-44. "Horizontal transmission of murine retroviruses." Competing interests: None declared |
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Alexander H Russell, Writer/artist/philosopher WC1N 1PE
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Regarding the impossibility of isolating 'HIV', Mr. Bennett unwittingly has completely given the game away: "It is not so much laziness as using superior techniques (faster, cheaper, more accurate) which render others redundant: but I accept that it means that EM of peripherally isolated HIV will likely never be done - because it doesn't need to be done." It most certainly does need to be done - but Mr. Bennett is right in stating it never will be done, but not for the reason he states. The fact is that the current crop of virtual virologists DARE not use the earlier, tried and trusted methods of viral isolation to find HIV in peripheral blood - because they know they would not find any particles at all. By affecting to disdain to use ultra centrifugation, peletting down etc. they can perpetuate the myth of HIV proliferation and pathogenicity by using indirect markers, as introduced by Robert Gallo, David Ho and others. In his book 'Virus Hunting - AIDS, Cancer & the Human Retrovirus: A Story of Scientific Discovery', Gallo readily admits that when he was working on HTLV1, a novel human retrovirus he suspected was the cause of adult T cell leukaemia, he was puzzled when he could never find any virus in the infected tissues of the elderly patients. It was he who suggested the use of surrogate markers as an acceptable alternative to actually finding and recovering virus using the traditional methods. Thus virtual virology was born -virologists were no longer required to demonstrate, with visual confirmation, the presence of virus in a patient's blood. They could just assume it was there by using antibody evidence, reverse transcription assays etc. Goodbye empirical observation, hello viral theology! 'HIV' research is not based upon hard science but is a matter of belief akin to religious faith: you cannot see the Holy Ghost but you are required to believe in it in order to belong to the club. However, as Peter Duesberg observed in his seminal paper published in Cancer Research (March 1st, 1987) viruses and other pathogens, typically when they cause a disease can be found at high titre, sufficient to cause cell destruction or intoxication at a faster rate than the body can replace them. The result is a disease condition. This just did not seem to be the case with HIV, which a) appeared to infect very few cells, and b) appeared to be restricted to latency by the antibody response. The apparent inactivity of 'HIV' worried those who sought to blame a retrovirus for 'AIDS', and that is what led David Ho and others to the theory behind 'viral load' testing. This purported to show that far from being an indolent virus restricted to latency by the immune system, HIV was hyperactive, creating billions of new particles daily, whilst the body simultaneously created billions of new cells to counter the viral proliferation. Ho was not bothered that such huge HIV titres had never been observed, nor the fact that the hallmark of HIV infection, if the experts were correct, should be the disappearance of cells, not a massive increase. Once again, it was left to Peter Duesberg to debunk a ridiculous, but still widely believed hypothesis, in a fully referenced letter he wrote with his colleague Harvey Bialy to Nature, which was grudgingly published in a much edited form. ("HIV an illusion" Nature 375: 197, 18 May 1995.) In their letter they point out that the methodology used by Ho et al and Wei et al, in two papers published in the same edition of Nature, grossly overestimated the numbers of viral particles claimed to be in a ml of plasma. "Here we would point out only that the central claim of the Ho et al and Wei et al papers-that 105 HIV virions per ml plasma can be detected in AIDS patients with various nucleic-acid amplification assays is misleading. The senior author of the Wei et al. paper has previously claimed that the PCR method they used overestimates by at least 60,000 times the real titer of infectious HIV: 100,000/60,000 is 1.7 infectious HIVs per ml, hardly the "virological mayhem" alluded to by Wain-Hobson. Further, Ho and a different group of collaborators have just shown that more than 10,000 "plasma virions," detected by the branched-DNA amplification assay used in their Nature paper, correspond to less than one (!) infectious virus per ml. And infectious units, after all, are the only clinically relevant criteria for a viral pathogen." (My emphasis) Eminent electronmicroscopist Prof. Etienne de Harven*, in criticising the loss of precision due to the abandonment of EM in identifying and quantifying viruses, pointed out that the pretext they used for their abandonment (like Mr. Bennett) was that EMs were unnecessary, time consuming and too costly: de Harven stated: "Dangerously enough, EM was progressively dismissed in retrovirus research after 1970. Molecular biologists started to rely exclusively on various 'markers', and what was sedimenting in sucrose gradient at density 1.16 gm/ml was regarded as 'pure virus'. It is only in 1997, after fifteen years of intensive HIV research, that elementary EM controls were performed, with disastrous results." These "disastrous results" published in Virology (Gluschankof et al. and Bess et al.) did not show purified/isolated 'HIV' but a mass of cellular debris and microvesicles with three ambiguous dots which were arbitrarily identified as 'HIV'. De Harven concludes: "In conclusion, and after extensive reviewing of the current AIDS research literature, the following statement appears inescapable: neither electron microscopy nor molecular markers have so far permitted a scientifically sound demonstration of retrovirus isolation directly from AIDS patients." (REMARKS ON METHODS FOR RETROVIRAL ISOLATION by Etienne de Harven, Continuum, Spring 1998.) If the methods of viral detection using indirect 'markers' Mr. Bennett trusts really work, then it is axiomatic that using the earlier methodology will only confirm their findings. It is time to clear up this point before 'HIV' research becomes even more irrational and ludicrous. Surely it would be worth while to spend a mere three or four days with basic EM equipment to confirm visually the results obtained by using Mr. Bennett's "superior techniques"? Hence, Mr. Bennett's statement is absurd and pure madness: "I accept that it means that EM of peripherally isolated HIV will likely never be done - because it doesn't need to be done." It does need to be done and urgently: can Mr. Bennett do it - and prove that 'HIV' exists? *Etienne de Harven worked in electron microscopy (EM) primarily on the ultra-structure of retroviruses throughout his professional career of 25 years at the Sloan Kettering Institute in New York and 13 years at the University of Toronto. In 1959 he was the first to report on the EM of the Friend virus in murine (mouse) leukaemia, and in 1960 to coin the word "budding" to describe steps of virus assembly on cell surfaces. Competing interests: None declared |
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