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Medical Forum / Diseases and Disorders / AIDS / October 2005Questions For Chris Noble and Other HIV Pundits
Anthony Fauci has published in Science that only 1 in 100 to 1 in 1000 T cells are ever infected in antibody-positive people with and without AIDS (Schnittman et al 1989). A British group, Simmonds et al., reports even lower rates of infection, namely 1 in 500 to 1 in 3000. Even more importantly regarding the "activity" of HIV under these conditions, they report that only 1 in 10,000 to 100,000 cells express some HIV RNA (Simmonds et al 1990). How would HIV-infected people lose their T-cells, except for the 1 in 100 to 1000 that are infected? According to conventional logic something other than HIV must kill the 99% to 99.9% uninfected T-cells of HIV-infected people. How do you explain T-cell "pathogenicity" by a virus that is making RNA in only 1 out of 10,000 to 100,000 cells? >Anthony Fauci has published in Science that only 1 in 100 to 1 in 1000 T >cells are ever infected in antibody-positive people with and without AIDS [quoted text clipped - 9 lines] >people. How do you explain T-cell "pathogenicity" by a virus that is >making RNA in only 1 out of 10,000 to 100,000 cells? Actually, these are incredibly important questions and quite a lot has been learned since 1990, both about the pathogenesis of HIV and the pathogenesis of AIDS, not to mention immunology in general. This may relate to some fundamental mechanisms: 1) sequestration of T cells into the lymphoid tissue (nodes, spleen, etc.); 2) modestly reduced thymic output of naive CD4+ cells; 3) various mechanisms of cell "suicide." There is clearly a much higher rate of programmed cell death (apoptosis) among uninfected CD4+ lymphocytes in HIV+ individuals than HIV negative people. These include: a) oxidative stress; b) immunological deception where antigen-presenting cells that are infected induce CD4 cells to become anergic and, upon subsequent stimulation, undergo apoptosis; c) autoimmune phenomena (tho this appears to be a minor component if relevant at all, unlike HCV infection where cryoglobulinemia, for example, represents a form of autoimmunity that afflicts a significant minority of HCV+ individuals); d) induction of inflammatory cytokines such as TNF, IL1b, IL6; and; 4) interaction of HIV proteins, notably gp120, tat and nef with apoptotic consequences. In addition, a family of smoldering, quiescent CD4 cells appears to sustain the ongoing replication of HIV even in the presence of highly active therapy. The area is one of debate to this day (see abstract below). But the evidence we do have has therapeutic implications. For example, to the extent that glutathione depletion may play a pivotal role in T cell loss due to oxidative stress, use of agents such as N-acetylcysteine, whey proteins, alpha lipoic acid and silymarin may all offset this loss. Or, for example, the use of carnitine may help to normalize high levels of tumor necrosis factor (TNF). THESE are important questions. George M. Carter ** Herbeuval JP, Grivel JC, Boasso A, Hardy AW, Chougnet C, Dolan MJ, Yagita H, Lifson JD, Shearer GM. CD4+ T cell death induced by infectious and noninfectious HIV-1: role of type I interferon-dependent, TRAIL/DR5-mediated apoptosis. Blood. 2005 Jul 26; [Epub ahead of print] Experimental Immunology Branch, NCI, NIH, Bethesda, MD, USA. Both direct and indirect mechanisms have been proposed to contribute to the unresolved issue of CD4(+) T cell depletion that results from HIV-1 infection. We recently reported that plasma levels of TNF-Related Apoptosis-Inducing Ligand (TRAIL) are elevated in HIV-1-infected patients, and correlate with viral load. The present study investigates the expression of TRAIL death receptor 5 (DR5) in PBMC from HIV-1-infected patients and its role in CD4(+) T cell death. DR5 expression was elevated and associated with the apoptotic marker Annexin V. Apoptosis was reduced in patients' CD4(+) T cells when cultured with anti-DR5 antibody. CD4(+) but not CD8(+) T cells from uninfected donors expressed TRAIL, DR5 and activated caspase-3 when cultured with infectious or noninfectious HIV-1, resulting in preferential apoptosis of CD4(+) T cells. TRAIL, caspase-3 expression and apoptosis were type I interferon-dependent. Induction of apoptosis and DR5 expression required gp120-CD4 interaction. Finally, we analyzed DR5 expression by CD4(+) T cells in HAART treated patients. The decreased viral loads and increased CD4 counts of HAART-responsive patients were associated with a decrease in DR5 mRNA expression by CD4(+) T lymphocytes. We propose a novel model in which a type I interferon-regulated TRAIL/DR5 mechanism induces apoptosis of HIV-1-exposed CD4(+) T cells. Mr. Carter, you outdid yourself. You managed to come up with some reasonable stuff. Actually, your answer is better than Mr. Noble's. The paper you quote is a good one. No glaring flaws this time. Muchbetter than the 29 whiffs of hot air your buddy Mr. Stein fixed me up with. It is obvious that apoptosis is the central issue. If apoptosis is stimulated, the average number of T-cells will go down. This phenomenon has been known for a long time in the case of red cells (hemolytic anemia), but it has only become an object of study since AIDS was invented. Obviously, there is stil a lot to learn about the subject, and it's up to the immunologists to provide the answers. >"We recently reported that plasma levels of TNF-Related Apoptosis-Inducing Ligand (TRAIL) are elevated in HIV-1-infected patients, and correlate with viral load." That may be true, but then the question arises: What does this viral load mean? Certainly not virus particles in the circulation (otherwise it would be possible to isolate them). What we call "viral load" consists really of small pieces of RNA, and we really don't know where they're coming from. According to the HIV-dogma, they represent HIV, but there is no proof of that. Summarizing, we can start from the basic premise that there are people with low CD4+ T-cell counts. Not even a denialist will deny that. That, and nothing else, is our starting point. If we search for what causes these depressed CD4 levels, apoptosis seems like a good candidate. But what causes the life cycle of the lymphocytes to get shortened? That question is still open. but it is almost certainly an internal matter of the human body. >"We propose a novel model in which a type I interferon-regulated TRAIL/DR5 mechanism induces apoptosis of HIV-1-exposed CD4(+) T cells." Why "HIV-1-exposed cells? Because HIV is mandatory. In a free world, the investigators would be free to look for a factor that makes CD4+ cells more susceptible to apoptosis. In the world we're living in, it has been decreed that HIV is that factor. In my view, the starting point is: "Some people have a depressed CD4+ count. That is a hard fact that everybody can verify, and nobody can deny. What causes this phenomenon?" According to the orthodoxy, the starting point is: "We have this here virus (we'll call it HIV), and it is supposed to kill you. How can we hook it up with low CD4+ counts?" I hope this will make people think. And if they do, they'll have you to thank for it, Mr. carter. >Mr. Carter, you outdid yourself. You managed to come up with some >reasonable stuff. Actually, your answer is better than Mr. Noble's. [quoted text clipped - 16 lines] >That may be true, but then the question arises: What does this viral load >mean? It reflects the amount of virus per milliliter of blood or other volume or tissue. >Certainly not virus particles in the circulation (otherwise it >would be possible to isolate them). Incorrect. HIV has been isolated. >What we call "viral load" consists >really of small pieces of RNA, and we really don't know where they're >coming from. YOU don't know. Most scientists have found that the segments that are amplified via PCR or other technology reflects HIV activity. Nothing endogenous about it Indeed, this is not the only way HIV has been visualized. Some fascinating film clips of gag proteins coalescing at the site of the "immunological synapse" are quite remarkable. >According to the HIV-dogma, they represent HIV, but there is >no proof of that. There is no PROOF of anything in biology ever. There is, however, strong evidence that constitutes a reasonable probability. >Summarizing, we can start from the basic premise that there are people >with low CD4+ T-cell counts. Not even a denialist will deny that. That, >and nothing else, is our starting point. That and nothing else? Like how did that situation arise? >If we search for what causes these depressed CD4 levels, apoptosis seems >like a good candidate. But what causes the life cycle of the lymphocytes >to get shortened? That question is still open. but it is almost certainly >an internal matter of the human body. LOL. Well, at least you had the guts to suggest something, however abjectly lame. >>"We propose a novel model in which a type I >interferon-regulated TRAIL/DR5 mechanism induces apoptosis of [quoted text clipped - 4 lines] >more susceptible to apoptosis. In the world we're living in, it has been >decreed that HIV is that factor. Bullshit. People are looking for reasons for apoptosis all over the place for other conditions. >In my view, the starting point is: "Some people have a depressed CD4+ >count. That is a hard fact that everybody can verify, and nobody can [quoted text clipped - 3 lines] >virus (we'll call it HIV), and it is supposed to kill you. How can we >hook it up with low CD4+ counts?" It's "hooked up" to CD4+ lymphocytes in part because HIV infects them. Duh. Look up interactions of nef, tat and gp120 with CD4. >I hope this will make people think. And if they do, they'll have you to >thank for it, Mr. carter. By all means. It would be really LOVELY to see some people actually think. But so far, all we have is a whole hell of a lot of dithering, handwaving and bullshit. George M. Carter >"It reflects the amount of virus per milliliter of blood or other volume or tissue." No. It reflects the amount of SOMETHING per milliliter of blood or other volume or tissue. >"Incorrect. HIV has been isolated." The whole world is searching for the paper describing this isolation, Mr. Carter. Including Kary Mullis. I asked you for it several times, and I think Paul did too. Why are you hiding it? >"YOU don't know. Most scientists have found that the segments that are amplified via PCR or other technology reflects HIV activity. Nothing endogenous about it Indeed, this is not the only way HIV has been visualized. Some fascinating film clips of gag proteins coalescing at the site of the "immunological synapse" are quite remarkable." Oh, sure. They have never seen an HIV particle, but they know exactly what its activity is. Yes, you showed me one of those fascinating film clips before. But one does not realize what it is unless someone is standing behind you, hitting you on the head with a stick, promising to stop only after you repeat after him: "These are gag proteins coalescing. And these gag proteins com from HIV." How the hell can they heap so much data on a virus they can't even show to exist? And get away with it for 20 years? >"There is no PROOF of anything in biology ever. There is, however, strong evidence that constitutes a reasonable probability." Yeah. About as much probability as "possession by the devil". >"That and nothing else? Like how did that situation arise?" Where did I say "and nothing else"? The only hard facts we have are: Some people have low CD4-counts. Some people get sick, and some people die. Start from there. Don't postulate some stupid virus that should be responsible for all of this. >"Bullshit. People are looking for reasons for apoptosis all over the place for other conditions." Are they really? GOOD! Because the virus theory is ridiculous. >"It's "hooked up" to CD4+ lymphocytes in part because HIV infects them. Duh. Look up interactions of nef, tat and gp120 with CD4. Duh indeed. Because there IS no virus. (and if you think there is, show me!) Those nice proteins all have their origin in the human body itself. >>"It reflects the amount of virus per milliliter of blood or other volume >or tissue." > >No. It reflects the amount of SOMETHING per milliliter of blood or other >volume or tissue. This has been all gone over ad nauseam on BMJ. And guess what? HIV exists. Regardless of how much you'd like to pretend is doesn't. Just like flu virus exists. Or Semliki Forest Virus. They use similar techniques to identify LOTS of pathogens. To claim HIV doesn't exist means NO virus or pathogen exists. Is that what you think? [QUOTE]"And guess what? HIV exists. Regardless of how much you'd like to pretend is doesn't. Just like flu virus exists. Or Semliki Forest Virus. They use similar techniques to identify LOTS of pathogens. To claim HIV doesn't exist means NO virus or pathogen exists."[/QUOTE] It doesn't mean that at all. The other viruses you mention have been isolated and identified. HIV has not. [QUOTE]"This has been all gone over ad nauseam on BMJ."[/QUOTE] Indeed it has. And you didn't learn anything from it? >[QUOTE]"And guess what? HIV exists. Regardless of how much you'd like to >pretend is doesn't. Just like flu virus exists. Or Semliki Forest Virus. [quoted text clipped - 4 lines] >It doesn't mean that at all. The other viruses you mention have been >isolated and identified. HIV has not. Really? Prove it. Based on what?? >"Really? Prove it. Based on what??" Based on the paper I already quoted (to Mr. Noble I believe) quite some time ago, on this forum. Influenza virus was first isolated in 1933. Here's a presentation that is perhaps a good illustration that we are talking about real viruses here: http://www.uncpeds.org/senior%20presentations/Influenza_files/frame.htm Semliki Forest Virus was first isolated in 1944. I can't find the paper on the Web, but it is definitely in the university libraries. And HIV? An ear-shattering nothing! >>"Really? Prove it. Based on what??" > >Based on the paper I already quoted (to Mr. Noble I believe) quite some >time ago, on this forum. The URL you cite is not a paper. >Influenza virus was first isolated in 1933. >Here's a presentation that is perhaps a good illustration that we are >talking about real viruses here: > >http://www.uncpeds.org/senior%20presentations/Influenza_files/frame.htm This doesn't provide the methodology. >Semliki Forest Virus was first isolated in 1944. >I can't find the paper on the Web, but it is definitely in the university >libraries. Your claims are not credible. >And HIV? An ear-shattering nothing! According to you. Once again, you utterly fail to convince. George M. Carter >Here's a presentation that is perhaps a good illustration >that we are talking about real viruses here: http://www.uncpeds.org/senior%20presentations/Influenza_files/frame.htm Good god, you are now using slide presentations of cartoons as evidence for a virus???? Where are the scientific references? I think the EMs of "flu" represent microvesicles. Can you prove me wrong? Why do you accept only the evidence you wish to see? > Duh indeed. Because there IS no virus. (and if you think there is, show > me!) Those nice proteins all have their origin in the human body > itself. http://hiv-web.lanl.gov/content/hiv-db/COMPENDIUM/1997/partIII/Gelderblom.pdf see also http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=1433527 and http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=nucleotide&val=9409797 for the genetic sequence of a HIV isolate. now use blast http://www.ncbi.nlm.nih.gov/blast/ to search for any alignments with human DNA. Chris Noble Yes, I'm familiar with the Gelderblom papers. At best their pictures show *particles*. Whether they are really retroviral particles is never shown. They could be microvesicles from the host cells, they could be anything. The genetic "HIV sequences" of "HIV isolates" vary all over the map. I don't do this often, but let me cut and paste a paragraph from Neville Hodgkinson's book: "The theory (there is no virus) explains why no two identical "HIV"s have been found, even from the same individual. When immune cells are stimulated in the laboratory, genes naturally present can be triggered into reproducing and recombining. By convention, certain packages of these genes have been interpreted as meaning the presence of HIV. But since the genes are individual to their host, rather than from a unique virus, they differ to such an extent that scientists have been forced to develop theories that HIV constantly mutates, forming what is described as a "quasi-species". The "complete HIV genome" (and this is me again) is like a jigsaw puzzle put together by mentally underprivileged children. > Yes, I'm familiar with the Gelderblom papers. At best their pictures show > *particles*. Whether they are really retroviral particles is never shown. [quoted text clipped - 16 lines] > The "complete HIV genome" (and this is me again) is like a jigsaw puzzle > put together by mentally underprivileged children. Nice bit of personal opinion but where's the Blast sequences to back up your statements? Hodgkinson is as credible as you are, which is sadly not saying much. Quote us the data from his book that backs up your quote with genetic data and some one might pay attention to you other then commenting on your ignorance. Gary Stein > Yes, I'm familiar with the Gelderblom papers. At best their pictures show > *particles*. Whether they are really retroviral particles is never shown. [quoted text clipped - 13 lines] > theories that HIV constantly mutates, forming what is described as a > "quasi-species". Contrary to Neville Hodgkinson's claim Manfred Eigen introduced the concept of a quasi-species before the discovery of HIV. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=593400&query_hl=4 Have you been able to come up with any references that support your claim that RNA viruses such as poliovirus do not have high mutation rates? > The "complete HIV genome" (and this is me again) is like a jigsaw puzzle > put together by mentally underprivileged children. Brilliant critique. Do you have any thing else other than your opinion? Chris Noble http://www.umich.edu/~urecord/9293/Mar01_93/19.htm Only 500 books were burned. How did the fire cause the damage to the other 10,000 books? Would dissidents claim that someone lighting a fire didn't really cause 10,000 books to be damaged? You may also be interested in reading this. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1 0208914&dopt=Citation In the case of Dengue hemorrhagic fever it is the host immune response that does the damage not the dengue virus directly lysing cells. It is Duesbergian Dogma that viruses can only cause disease by directly lysing cells. Dissidents may see Duesberg as an authority but viruses do not blindly follow his decrees on how they should behave. Chris Noble Mr. Noble, you're just the man I wanted to find. Yes, when viruses do actual damage, it's always by directly lysing cells. That's old virology wisdom, not Duesberg dogma. There are some examples of viruses lingering awhile (lysogeny of bacteriophages, latent period of Herpes viruses), but during these inactive periods, the virus does not cause any harm. And even those latent periods are nothing like the totally mythical incubation time of 10 years for 'HIV' to strike. I've had Dengue fever. It cured itself in a few days. This happened just during the time I was on the team at the Health Dept. that was responsible for eradicating the epidemic. We got rid of it by spraying the whole city and killing off the mosquitos. Not very elegant, but it worked, especially in a political sense. These viral epidemics burn themselves out in a short period. You don't really have to do anything, but for political reasons it may be better to make it appear that you are taking action. That's why HIV-disease is so anomalous. These immuno-suppression cases are behaving in such a weird way that it is imposible to believe they are caused by a virus - any virus. > Mr. Noble, you're just the man I wanted to find. > Yes, when viruses do actual damage, it's always by directly lysing cells. [quoted text clipped - 9 lines] > and killing off the mosquitos. Not very elegant, but it worked, > especially in a political sense. What did you spray with and when did this occur? For someone who is so concerned about the dangers of ARV it is surprising to hear that he is comfortable with spraying an entire city with very toxic chemical insecticides. It is equally strange to hear some one who claims that politics is to blame for a world wide conspiracy to kill people i.e. the so called "HIV myth" saying that the politics of spraying were more important then the health impact of said spraying. It seems your a bit of hypocrite there Mr. Claster. > These viral epidemics burn themselves out in a short period. You don't > really have to do anything, but for political reasons it may be better to > make it appear that you are taking action. That's why HIV-disease is so > anomalous. These immuno-suppression cases are behaving in such a weird > way that it is imposible to believe they are caused by a virus - any > virus. You've already mentioned Herpes, how about the version of the Hepatitis virus that you do admit is real? Your ignorance about HIV is made apparent in almost everyone of your posts. HIV is not inactive during a patients asymptomatic period what ever gave you the idea that it is? Gary Stein >"What did you spray with and when did this occur? For someone who is so concerned about the dangers of ARV it is surprising to hear that he is comfortable with spraying an entire city with very toxic chemical insecticides. It is equally strange to hear some one who claims that politics is to blame for a world wide conspiracy to kill people i.e. the so called "HIV myth" saying that the politics of spraying were more important then the health impact of said spraying. It seems your a bit of hypocrite there Mr. Claster." We sent up a plane and sprayed the city of San Juan, Puerto Rico with Malathione. This was in 1977. And no, I'm not proud of it. The reason I mentioned it is to draw attention to the fact that these actions by Departments of Health always have a political background. My boss, the Assistant Secretary of Environmental Health was under heavy pressure "to do something". So something was done. Now I call your attention to the early eighties, when gay men were dying from rare unexpected diseases, and there was a strong clamoring "to do something" about the "epidemic". Well, the Reagan administration dragged its feet for a long time. Until the pharma industry could be convinced that there was money to be made by scaring the whole population with the lie that everybody could get "it". Then the government "did something". And I don't like what they did. I'm trying to educate you as to how governmental agencies work, Mr. Stein. And then you call me hypocritical. That ain't nice. > Mr. Noble, you're just the man I wanted to find. > Yes, when viruses do actual damage, it's always by directly lysing cells. > That's old virology wisdom, not Duesberg dogma. You still haven't managed to come up with any references for your claims that RNA viruses don't generally mutate. "Godschalk says" is not science. It is your opinion. It is worth as much as your opnion on whether RNA viruses mutate. Chris Noble >"You still haven't managed to come up with any references for your claims that RNA viruses don't generally mutate." ??? I beg your pardon?!! I never claimed RNA viruses don't generally mutate. I explained this several times, but here it is again: A complex virus such as Influenza has a segmented genome (more than one RNA chain) That means recombinations can occur fairly easily. That does not mean that a simple virus cannot mutate. But those simple viruses, such as Polio, or a retrovirus, have a smaller genome, and the virus needs all of it just to reproduce. Now mutation is a random event. There is no intelligence behind it. So for a small virus, any mutation will easily lead to a mutant that cannot reproduce anymore, or produces a coat protein that lacks the ability to infect target cells. The large viruses, on the other hand (Flu, Pox, Herpes), have some room to "play around", and can yield mutants that are viable. To assume that there are retroviruses that can perform rapid mutation, just because it suits them, is wrong thinking. >>"You still haven't managed to come up with any references for your claims >that RNA viruses don't generally mutate." [quoted text clipped - 13 lines] >that can perform rapid mutation, just because it suits them, is wrong >thinking. It may appear to be "wrong thinking" from a 1938 perspective, but with modern techniques, it is more readily possible to evaluate synonymous and nonsynonymous changes in a viral genome. It is not a matter of "assuming" that a retrovirus can mutate; it has been demonstrated that this can be done with variable but not totally abrogating effects on viral fitness. George M. Carter > I've had Dengue fever. It cured itself in a few days. You have not had Dengue hemorrhagic fever. http://www.nlm.nih.gov/medlineplus/ency/article/001374.htm "Dengue fever should not be confused with Dengue hemorrhagic fever, which is a separate disease and frequently fatal." http://www.nlm.nih.gov/medlineplus/ency/article/001373.htm "Dengue hemorrhagic fever is a severe, potentially fatal infection that occurs when someone with immunity to one type of Dengue virus is infected by a different type. It is spread by certain mosquitoes (Aedes aegypti) which bite primarily during the day. See also Dengue fever." "Risk factors for dengue hemorrhagic fever include having antibodies to dengue virus from prior infection and being younger than 12, female, or Caucasian." Chris Noble >"Dengue hemorrhagic fever is a severe, potentially fatal infection that occurs when someone with immunity to one type of Dengue virus is infected by a different type. It is spread by certain mosquitoes (Aedes aegypti) which bite primarily during the day." I know. This was the form people were scared with, to show how forceful and efficient their Health Department could be. I was there when it hit. I was part of the government team that took action in 1977. We eradicated the mosquitos (although an entomologist said it was the wrong thing to do; and I think he was right. But politics is politics). Nobody got the hemorrhagic form of Dengue. I didn't either. >I've had Dengue fever. Who told you that?? Did they isolate the virus? Prove it. I hope it wasn't a serological diagnosis....tut, tut! (It seems dengue serology falls somewhat short of the standards for HIV) http://cdli.asm.org/cgi/content/full/5/1/7 >>"I've had Dengue fever." >"Who told you that??" When you have Dengue fever, nobody has to tell you. You just feel it. >"Did they isolate the virus? Prove it." Isolate the virus? From me? Ya gotta be kidding. Serological diagnosis? Give me a break! Do you really think I would get myself involved into all these useless procedures for a li'l ol' virus infection? Call a doctor for something that will go away by itself in a few days (as a virus that really exists does) ? That's what the poor suckers who have been scared by the AIDS propaganda do wrong: Instead of letting the health nazis perform all kinds of tests and "therapeutic" onslaughts on them, they should withdraw from the medical merriment to a safe and quiet place, and get themselves some TLC. I did. >>>"I've had Dengue fever." > [quoted text clipped - 14 lines] > from the medical merriment to a safe and quiet place, and get themselves > some TLC. I did. Smallpox goes away by it's self, really are you sure you want to say that? West Nile goes away by it's self, again are you sure you want to make that claim? The 1918 strain of Flu went away by it's self, are you sure you want to make that claim. Should I go on, you know as well as I do that the list of viruses that are able to kill a significant number of those infected is not a small list at all. Gary Stein Gary- Can you prove that either small pox, west nile, or the Flu of 1918 killed each and every person it infected that did not use any sort of virus treatment, including vaccination? If even 1 person used no treatment and survived any of these afflictions, then yes, the virus does just *go away*. Sincerely, Michael Kilduff " We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake" Dr. Kary Mullis, Nobel Laureate and inventor of Polymerase Chain Reaction. Mr. Noble- Thank you for your response. But what mechanism can you ascertain that HIV employs to kill CD-4's? If you want to state that a virus can infect such cells and kill them by indirect means, then why not blame AIDS and the destruction of CD-4's on other established viruses that infect these same cd-4's such as CMV, several hepesviruses, and hep B virus? Sincerely, Michael Kilduff " We know that to err is human, but the HIV/AIDS hypothesis is one hell of a mistake" Dr. Kary Mullis, Nobel Laureate and inventor of Polymerase Chain Reaction.
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