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Medical Forum / Diseases and Disorders / AIDS / May 2006HIV Pathogenesis & Immunology
I've taken the liberty of starting a new thread with this post from the Harper's thread. I used to post here a while back (when the late and sorely missed Carlton Hogan was still around, he once memorably called misc.health.aids the wild, wild west of HIV newsgroups), Anyway, I'm sufficiently fed up with the tiresome and potentially murderous activities of denialists that I figure it's worth at least trying to get them to argue with current science and immunology rather than some ancient dumb pronouncement from David Ho or Tony Fauci or whoever. So, here's my $0.02, if someone wants to take issue with these points go ahead, I'd be very happy to debate some HIV immunology. I'm not sure how this might work if you don't believe the virus exists at all, although we might be able to have an interesting discussion about why HIV-positive people with have T cell responses to a phantom while those that are uninfected don't (with the exception of the intriguing small group of highy exposed uninfected people that have HIV-specific T cell responses but no antibody responses). HIV/AIDS immunology in a non-exhaustive nutshell: AIDS is a viral disease of the immune system, the outstanding questions regarding pathogenesis are rooted in scientific ignorance of how the human T cell immune system actually works. HIV infection causes unique immunological peturbations which are not mirrored by malnourishment, drug abuse or anything else. The strongest predictor of disease progression is not viral RNA copies of CD4 T cell counts in peripheral blood, it's the level of IMMUNE ACTIVATION. Immune activation correlates with depletion of the naive CD4 and CD8 T cell pools (the depletion of which also correlates with the onset of clinically symptomatic immunodeficiency), which is also paralleled by a spreading dysfunction among memory CD4 and CD8 T cells, eventually leading to the loss/anergy of recall responses to common pathogens (PCP, MAC, etc.). Combination antiretroviral therapy, for all it's toxicities and limitations, suppresses immune activation, increases naive CD4 and CD8 T cell counts and typically restores functional memory T cell responses to opportunistic pathogens (allowing maintenance therapy for such pathogens to be discontinued). There are rare cases of things like PCP in people with relatively high peripheral blood T cell counts and these are associated with prolonged defects in the PCP-specific memory T cell response. The growing scientific understanding of T cell homeostasis (how T cell pools are maintained in the body) suggests plausible mechanisms by which persistent low level T cell activation can eventually lead to frank immunodeficiency (a mouse model has even been developed which recapitulates many features of HIV-related immune dysfunction by overexpressing the costimulatory molecule CD70). As immunologist Zvi Grossman has pointed out, there is no need for HIV to be cytopathic to CD4 T cells for it to cause disease, because activated T cells are inherently short-lived (~1-2 days) whether they are infected or not. HIV essentially feeds off the immune system's attempts to respond to it by preferentially infecting HIV-specific CD4 T cells which are critical for the development of effective CD8 and B cell & antibody reponses. I have yet to see any denialist information that actually attempts to address this current understanding of immunology as it relates to HIV infection, all the arguments (including those in the dismal Celia Farber outing in Harper's) are directed at literature that was published 10-20 years ago (no immunologists give any credence to David Ho's "tap and drain" hypothesis of HIV pathogenesis anymore, nor does the majority of the HIV research field). I should also maybe add that if you want to compare the immunological effects of HIV infection with malnourishment or drug addiction there are studies in PubMed, analyses of individuals with severe malnourishment due to anorexia nervosa for example (there are some similarities but a lot of differences i.e. peripheral blood CD4 T cell counts are reduced but nowhere near as dramatically, there's reduced immune activation, reduced CD8 T cell counts, no opportunistic infection and the abnormalities resolve rapidly upon refeeding). There is no evidence I can find of any recreational drug having persisent effects on T cell populations (there are, however, some preliminary suggestions that crystal meth might). Oh, and immune activation also likely explains the easier transmission of HIV in settings where the enviromental pathogen load is high e.g. Africa (see abstract below) Here are some cites that might be helpful: Nat Immunol. 2003 Jan;4(1):49-54. Epub 2002 Dec 9. Lethal T cell immunodeficiency induced by chronic costimulation via CD27-CD70 interactions. Tesselaar K, Arens R, van Schijndel GM, Baars PA, van der Valk MA, Borst J, van Oers MH, van Lier RA. Laboratory for Experimental Immunology, Academic Medical Center, P.O. Box 22700, 1100DD Amsterdam, The Netherlands. It has been proposed that HIV-1, in addition to directly infecting and killing CD4+ T cells, causes T cell dysfunction and T cell loss by chronic immune activation. We analyzed the effects of chronic immune activation in mice that constitutively expressed CD70, the ligand for the tumor necrosis factor receptor family member CD27, on B cells. CD70 transgenic (CD70 Tg) mice showed a progressive conversion of naive T cells into effector-memory cells, which culminated in the depletion of naive T cells from lymph nodes and spleen. T cell changes depended on continuous CD27-CD70 interactions and T cell antigen receptor stimulation. Despite this hyperactive immune system, CD70 Tg mice died aged 6-8 months from Pneumocystis carinii infection, a hallmark of T cell immunodeficiency. Thus, persistent delivery of costimulatory signals via CD27-CD70 interactions, as may occur during chronic active viral infections, can exhaust the T cell pool and is sufficient to induce lethal immunodeficiency. 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 Apr;8(4):319-23 Leng Q, Borkow G, Weisman Z, Stein M, Kalinkovich A, Bentwich Z. Immune activation correlates better than HIV plasma viral load with CD4 T-cell decline during HIV infection. J Acquir Immune Defic Syndr. 2001 Aug 1;27(4):389-97. Koesters SA, Alimonti JB, Wachihi C, Matu L, Anzala O, Kimani J, Embree JE, Plummer FA, Fowke KR. IL-7Ralpha expression on CD4(+) T lymphocytes decreases with HIV disease progression and inversely correlates with immune activation. Eur J Immunol. 2006 Feb;36(2):336-44. Hazenberg MD, Otto SA, van Benthem BH, Roos MT, Coutinho RA, Lange JM, Hamann D, Prins M, Miedema F. Persistent immune activation in HIV-1 infection is associated with progression to AIDS. AIDS. 2003 Sep 5;17(13):1881-8 Messele T, Brouwer M, Girma M, Fontanet AL, Miedema F, Hamann D, Rinke de Wit TF. Plasma levels of viro-immunological markers in HIV-infected and non-infected Ethiopians: correlation with cell surface activation markers. Clin Immunol. 2001 Feb;98(2):212-9. Hazenberg MD, Stuart JW, Otto SA, Borleffs JC, Boucher CA, de Boer RJ, Miedema F, Hamann D. T-cell division in human immunodeficiency virus (HIV)-1 infection is mainly due to immune activation: a longitudinal analysis in patients before and during highly active antiretroviral therapy (HAART). Blood. 2000 Jan 1;95(1):249-55. Hazenberg MD, Otto SA, Cohen Stuart JW, Verschuren MC, Borleffs JC, Boucher CA, Coutinho RA, Lange JM, Rinke de Wit TF, Tsegaye A, van Dongen JJ, Hamann D, de Boer RJ, Miedema F. Increased cell division but not thymic dysfunction rapidly affects the T-cell receptor excision circle content of the naive T cell population in HIV-1 infection. Nat Med. 2000 Sep;6(9):1036-42. Roederer M, Dubs JG, Anderson MT, Raju PA, Herzenberg LA, Herzenberg LA. CD8 naive T cell counts decrease progressively in HIV-infected adults. J Clin Invest. 1995 May;95(5):2061-6. Ullum H, Lepri AC, Victor J, Skinhoj P, Phillips AN, Pedersen BK. Increased losses of CD4+CD45RA+ cells in late stages of HIV infection is related to increased risk of death: evidence from a cohort of 347 HIV-infected individuals. AIDS. 1997 Oct;11(12):1479-85. AIDS. 2000 Sep 29;14(14):2083-92. Immune activation in africa is environmentally-driven and is associated with upregulation of CCR5. Italian-Ugandan AIDS Project. Clerici M, Butto S, Lukwiya M, Saresella M, Declich S, Trabattoni D, Pastori C, Piconi S, Fracasso C, Fabiani M, Ferrante P, Rizzardini G, Lopalco L. Cattedra di Immunologia, Universita di Milano, Italy. BACKGROUND: HIV infection in Africa is associated with immune activation and a cytokine profile that stimulates CCR5 expression. We investigated whether this immune activation is environmentally driven; if a dominant expression of CCR5 could indeed be detected in African individuals; and if R5 HIV strains would be prevalent in this population. METHODS: Freshly drawn peripheral blood mononuclear cells from HIV-uninfected African and Italian individuals living in rural Africa, from HIV-uninfected Africans and Italians living in Italy, and from HIV-infected African and Italian patients were analysed. Determinations of HIV coreceptor-specific mRNAs and immunophenotype analyses were performed in all samples. Virological analyses included virus isolation and characterization of plasma neutralizing activity. FINDINGS: Results showed that: immune activation is detected both in Italian and African HIV-uninfected individuals living in Africa but not in African subjects living in Italy; CCR5-specific mRNA is augmented and the surface expression of CCR5 is increased in African compared with Italian residents (CXCR4-specific mRNA is comparable); R5-HIV strains are isolated prevalently from lymphocytes of African HIV-infected patients; and plasma neutralizing activity in HIV-infected African patients is mostly specific for R5 strains. CONCLUSIONS: Immune activation in African residents is environmentally driven and not genetically predetermined. This immune activation results in a skewing of the CCR5 : CXCR4 ratio which is associated with a prevalent isolation of R5 viruses. These data suggest that the selection of the predominant virus strain within the population could be influenced by an immunologically driven pattern of HIV co receptor expression. I am afraid your post is rather wasted here. You are not likely to get anything vaguely resembling an intelligent response. Harvey Bialy is responding on this blog http://scienceblogs.com/aetiology/2006/02/discussion_of_the_padian_paper.php#com mentsArea although none of his responses show much intelligence. You may have fun with the Hank Barnes character. http://scienceblogs.com/aetiology/2006/02/discussion_of_the_padian_paper.php#com ment-18058 Chris Noble Thanks for the tips, it was a rather pompous salvo anyway! Just venting some frustration after reading the Celia Farber piece in Harper's. It's so surreal that they even published it, although it's also quite funny to read comments from people that think it means that the triumph of the denialists is upon us. I'll have a go at posting something on the aetiology blog. The Denialists have been saying that the "HIV/AIDS paradigm" is on the verge of toppling for about 20 years. Every year it is the same thing. Every year they recycle the same invalid arguments. I wouldn't bank on getting any intelligent responses on the Aetiology blog. The detailed "rebuttals" from Harvey Bialy gives you an example of the intelligence of the Denialist heirarchy. Chris Noble "The Denialists have been saying that the "HIV/AIDS paradigm" is on the verge of toppling for about 20 years. Every year it is the same thing. Every year they recycle the same invalid arguments." Yawn, ho-hum, boring old "denialists"...they keep recycling the same invalid aruguments...yet YOU keep spending so much of your time attempting to refute them. Are you just a fan of tedium and monotony? >"Just venting some frustration after reading the Celia Farber piece in Harper's." Frustration? I realy likes celia Farber's piece in Harper's. You'll get it thrown in your faces for years to come. >"You are not likely to get anything vaguely resembling an intelligent response." That's just because an intelligent response follows an intelligent post, which this was not. Oh gawd! An immunologist. A representative of an immature science where nobody knows what's going on, but everybody wants to dominate the whole biomedical field. Well, what your piece resembles most is the "Peter Palaver" (you know, from the same author who wrote "The Peter Principle") All the words have a distinct meaning, but the sentences make no sense at all. Lots of immunological jargon, to put off sensible people from responding. But let me pick on some items I do understand: >"I figure it's worth at least trying to get them to argue with current science and immunology rather than some ancient dumb pronouncement from David Ho or Tony Fauci or whoever." Ah, so. After we shot down Gallo, Ho, and Fauci (who was always called upon to replace Duesberg, to give a talk or an interview), you are ready to drop them. Now you come with "current science and immunology" as the definitive answer. Well, I've got news for you: Once we figure out what you're really saying, we'll shoot that down also. So your fellow poisoners and con artists can come up with yet another batch of then-current science. >"I'm not sure how this might work if you don't believe the virus exists at all," Neither do I. Where's the virus? As I understand it, you're taking a nothing, and wrap it in an immunological coat. >"although we might be able to have an interesting discussion about why HIV-positive people with have T cell responses to a phantom while those that are uninfected don't (with the exception of the intriguing small group of highy exposed uninfected people that have HIV-specific T cell responses but no antibody responses)." Right. But the thought would never enter your mind that what you call "HIV-positive" might have nothing to do with a virus, isn't it? Especially since the same effects can be observed in "HIV-negative" persons. >"AIDS is a viral disease of the immune system" That's off to a very unscientific start. You have no proof whatsoever that it's a viral disease. If you take this statement as an incontrovertible truth, you may wind up way off course. >"Immune activation correlates with depletion of the naive CD4 and CD8 T cell pools (the depletion of which also correlates with the onset of clinically symptomatic immunodeficiency), which is also paralleled by a spreading dysfunction among memory CD4 and CD8 T cells, eventually leading to the loss/anergy of recall responses to common pathogens (PCP, MAC, etc.)." Hm! Sounds fishy. But I'll take your word for it for the moment, because what's coming now is much worse: >"Combination antiretroviral therapy, for all it's toxicities and limitations, suppresses immune activation, increases naive CD4 and CD8 T cell counts and typically restores functional memory T cell responses to opportunistic pathogens (allowing maintenance therapy for such pathogens to be discontinued). There are rare cases of things like PCP in people with relatively high peripheral blood T cell counts and these are associated with prolonged defects in the PCP-specific memory T cell response." I'm glad you acknowledge the toxicities and limitations, because that's what concerns me most about this whole AIDS business. Well, I guess you know your imunology, but I still get the impression that none of the immunologists really know what's going on, but at least they have a name for everything they observe. But tell me: When you read your own paragraph that I quoted above, do you see any need for a virus named HIV? You describe pure immunological events. Are there any indications at all that there's a virus at play? >"As immunologist Zvi Grossman has pointed out, there is no need for HIV to be cytopathic to CD4 T cells for it to cause disease, because activated T cells are inherently short-lived (~1-2 days) whether they are infected or not." OK, I accept the part about T-cells. The part about HIV is balderdash, horsefeathers, bunkum, fiddlesticks (and words to that effect). There is simply no need for HIV to cause disease; there are many other causes of pathogenesis. >"HIV essentially feeds off the immune system's attempts to respond to it by preferentially infecting HIV-specific CD4 T cells which are critical for the development of effective CD8 and B cell & antibody reponses." Ah, now I understand how you do it: First you write something that makes sense, or is at least halfway plausible. Then you follow up with the most resounding nonsense you can think of, hoping we'll swallow it all. How the hell do you know "HIV" preferentially infects "HIV-specific CD4 T-cells"? What *are* HIV-specific T-cells? On what evidence do you base your belief in HIV? And why would HIV (if such a beast exists) infect just a special kind of CD4 T-cells? >"I have yet to see any denialist information that actually attempts to address this current understanding of immunology as it relates to HIV infection," We're happy with any information we can get from the immunologists. But while immunologists know all about T-cells, they generally have a poor understanding of virology. Oyherwise they would know that immunology does not relate at all to "HIV infection". >"all the arguments (including those in the dismal Celia Farber outing in Harper's) are directed at literature that was published 10-20 years ago (no immunologists give any credence to David Ho's "tap and drain" hypothesis of HIV pathogenesis anymore, nor does the majority of the HIV research field)." Well, there used to be a time when literature that was published 10-20 years ago (or even 60 years ago) was still perfectly valid. Not in the AIDS era, unfortunately. "AIDS scientists" pose some outrageous theory. And when the dissidents knock it down and trample on it, the orthodoxy says, without a trace of embarrassment: "We knew that. We don't believe that anymore." Then they come up with a theory that's even more outrageous. >"I should also maybe add that if you want to compare the immunological effects of HIV infection with malnourishment or drug addiction there are studies in PubMed, analyses of individuals with severe malnourishment due to anorexia nervosa for example (there are some similarities but a lot of differences i.e. peripheral blood CD4 T cell counts are reduced but nowhere near as dramatically," Could be. But don't compare somebody with anorexia nervosa to the human wrecks that were entering the hospitals during the early eighties. Besides, the symptoms (and I guess also the immunological picture) of the early AIDS patients were rapidly aggravated by AZT monotherapy at high doses. I don't think I have time to go to the library to read all those papers. Your series of references already begins with an 8-author article (for an ordinary research paper, that's ridiculous!), and to make matters worse, it's from the AMC in Amsterdam. The abstract of the last paper in the series already gives me an idea of what to expect: Starting out with full faith in HIV as an infectious agent. Preconceptual science. HIV-positive people with have T cell responses to a phantom while those that are uninfected don't (with the exception of the intriguing small group of highy exposed uninfected people that have HIV-specific T cell responses but no antibody responses)." "Right. But the thought would never enter your mind that what you call "HIV-positive" might have nothing to do with a virus, isn't it? Especially since the same effects can be observed in "HIV-negative" persons." I was talking about T cell responses. The fact that T cell responses to all the proteins encoded by the HIV genome can be found in HIV infected people suggests that the virus has something to do with what the immune system is doing, no? The unique immunological peturbations of HIV infection - persistent immune activation, naive T cell depletion and memory T cell dysfunction - are not observed in uninfected or HIV negative people. Frankly, if you find the number of authors on a paper off-putting I don't think this is likely to be a very productive discussion. And if your fallback position is to desribe all human immunology as some kind of phenomilogical nonsense, well, I hope you have been careful to avoid all vaccines and therapies that are based in the science of human immunology. >"The fact that T cell responses to all the proteins encoded by the HIV genome can be found in HIV infected people suggests that the virus has something to do with what the immune system is doing, no?" Well, there is clearly "something going on" in seropositive people that is not found in seronegatives. But what does the test show? Antibodies to certain proteins. You say that these proteins are "encoded by the HIV genome". What proof can we find for that statement? To be sure that it's the "HIV genome" we're talking about, we first have to isolate the pure virus, so that the RNA can be extracted from it, and then look if the proteins in the test kits are really coded for by this viral RNA. But none of this has been accomplished. So the only conclusion we can draw at this moment is: There's something strange going on with people who test positive on this test, but we don't know yet what causes it. >"Frankly, if you find the number of authors on a paper off-putting I don't think this is likely to be a very productive discussion." I don't see why not. I am wary of those publications, but that doesn't mean I don't want to read them. It's a habit scientists developed in the past 20 years, and it can usually attributed to sloppy science. It's like making a quilt. A large number of authors is only justified if it's a monumental project where many people were needed to finish it. Look at old, classic papers, by Landsteiner for example. That was trailblazing work. But he published mostly anone. All these papers with 13 authors on occasion, only reflect the hunt for research grants. >"And if your fallback position is to desribe all human immunology as some kind of phenomilogical nonsense, well, I hope you have been careful to avoid all vaccines and therapies that are based in the science of human immunology." No, that is not really my fallback position. I do have respect for the science of immunology. It's still largely in the phenomenological stage, but we can expect major advancements. In one of my older posts I even recommended taking most of the wasted money away from the virologists, because they have made a complete mess of it, and giving more grant money to the immunologists. But they should stick with the things they know about, and develop those lines of inquiry further. They should ignore the "virus of the month" nonsense that appears with regularity on the front pages of the daily press. If the immunologists stick to their trade, I'm sure we will see some astounding progress in the life sciences. And by the way, yes I am careful with vaccines. But that is not the fault of the immunologists. I'm just a little leery of the chemicals they put in those vaccines as a preservative. Thimerosal (an organic mercury compound) for example. And besides there may be contaminating viruses in it. Those clerics in Nigeria may not have been bullshitting... >>"The fact that T cell responses to all the proteins encoded by the HIV >genome can be found in HIV infected people suggests that the virus has >something to do with what the immune system is doing, no?" > >Well, there is clearly "something going on" in seropositive people that is >not found in seronegatives. Wow. Brilliant. You kinda can't get around that one, huh? >But what does the test show? Antibodies to >certain proteins. Not ones found normally in the human body. Gosh. How do they get there. Perhaps...gosh...a VIRUS? That encodes a variety of structural and regulatory proteins that have been well characterized? George M. Carter Well the antibody tests correlate almost perfectly (with the exception I already noted of ESNs) with the presence of T cell responses to all nine proteins: Gag, Pol, Nef., Env, Tat, Rev, Vif, Vpr, Vpu. T cell responses are detected with exquisite specificity using new technologies called ELISpot, intracellular cytokine staining and tetramers. Although denialists have made up a bunch of stuff to try and explain away antibody responses by some kind of cross reactivity, they have yet to make something up to account for the T cell responses you can now detect using these assays. I'm sure they will eventually of course. Perhaps your position that it has not been demonstrated that these proteins are encoded by the HIV genome will be the explanation of choice!! They come from outer space! What would be of tremendous value at this point would be to have a moderated academic debate, which was considered essential in academia when such disagreements arose amongst those who could put forth a reasoned argument for considering an alternative to the "mainstream veiw" (such as "the world is flat"). The problem is that people like Fauci act like they were appointed by God to spread the Word of "HIV/AIDS," and will not agree to this kind of scrutiny. In the meantime, I renew my offer to be "infefected" with "HIV," but I also ask those who believe that "HIV causes AIDS" why they are so fearful of a true academic debate? Whenever I have seen tentative attempts at this, such as the Perth Group making the point about "molecular clones of HIV," it is always the "dissident" who makes by far the most sense, and they provide the detailed scientific analysis. Moreover, those who make the claim, such as that there is a "retrovirus" that "causes AIDS" are the ones who are under the burden of demonstrating that their claim is valid, after the scientific method has been employed towards this end. Instead, what we have are "correlations" and "markers." If "HIV" exissted and did the damage it is said to do, there would be direct evidence and it would be easy to explain exactly what is happening. Instead, it is impossible to do this, but on the other hand, it is very easy to look at the professional literature on immune system dsyfunctions and understand why people who were exposed to certain stressors developed "AIDS." So one of you "HIV/AIDS defenders" and myself can prove to the world what is really going on: I will be "infected by HIV," but otherwise not do anything stressful to my body. You will be exposed to the behaviors most of those who develop "AIDS" in the West engage in, such as extreme anitgenic exposure, poor nutrition, massive use of corticosteriors and antibiotics, etc. for 2 years, then put you on 3 years of AZT. We will see who lives longer, and who dies of a condition that looks very much like "AIDS." I am willing to put my life on the line here. Who among the true "HIV/AIDS" believers can say the same thing about their understanding of the scientific evidence? >What would be of tremendous value at this point would be to have a >moderated academic debate, which was considered essential in academia Oh f.ck you. Another a.shole whose lip flap the age-old tune of senseless flatulence masquerading as erudition. Montyjerk, there HAS been a HELL of a lot of very nice, delicate, high-falutin' academic debate discussing every tiny detail of the issues of HIV and AIDS. All the questions, queries and exhortations of the Denialists have been scrutinized, responded to and addressed. And HIV still exists, still causes AIDS. MANY far more and genuine questions remain, stretching from the virus to the global situation. But NONE of them have to do with any of the vacuous and vapid ditherings that come from the deranged likes of you. George M. Carter "The unique immunological peturbations of HIV infection - persistent immune activation, naive T cell depletion and memory T cell dysfunction - are not observed in uninfected or HIV negative people." Do you have a citation for this that is consistent with the scientific method? To be clear, what a scientist would need to do to confirm your claim is to find a few hundred people who have tested "HIV positive" but who are asymptomatic. Then, those people would have to be confined and all immunosuppressive agents known to science, including dietary ones, such as EPA (the fatty acid that is found in large amounts in fish oil), would have to be removed. No toxic drugs could be given to them. Then, we would wait and see if they develop "AIDS." We both know this has not been done, but if it is not, what we have here is circular logic. A person who is having "AIDS"-like symptoms, but who engaged in no activity that would "infect" him/her with "HIV" will not get the test, so he/she might go on to die, but it will be called a known "disease," instead of being called "AIDS," though all else is equal. If you can't see that this bears no resemblance to science, then you need to fear you lack of reasoning skills more than a virus that is most likely fictitious. "it is very easy to look at the professional literature on immune system dsyfunctions and understand why people who were exposed to certain stressors developed "AIDS."" Is it? Why don't you provide some cites that show "stressors" causing the immunological peturbations that are seen in HIV infection? I'd be particularly interested in the stressors that can cause an accumululation of memory HIV-specific CD8 T cells such that they end up representing the majority of the memory CD8 T cell pool. So, you need stressors that produce exact mimics of epitopes from all the proteins mentioned above: (Gag, Pol, Nef., Env, Tat, Rev, Vif, Vpr, Vpu). >"Why don't you provide some cites that show "stressors" causing the immunological peturbations that are seen in HIV infection?" While Montygram is doing that, why don't YOU look up sime references that show it is "HIV-infection" that causes the immunological perturbations? I've warned you before that it would be better to stick to immunological studies, Mr. Jeffery. If you ever want to make something out of your career, that is. Just leave the viral crap to the virologists. We'll be coming for them anyway when "Hatchet Day" rolls around. Amd by the way, these proteins (Gag, Pol, Nef, Env, Tat, Rev, Vif, Vpu, and Vpu) are all figments of the rich imaginations of the geneticists. There is nothing viral about them. "Amd by the way, these proteins (Gag, Pol, Nef, Env, Tat, Rev, Vif, Vpu, and Vpu) are all figments of the rich imaginations of the geneticists. There is nothing viral about them. " So why are they antigenic to the immune system such that they induce specific T cell and B cell responses? Are they figments of the T cell's imagination? >"So why are they antigenic to the immune system such that they induce specific T cell and B cell responses? Are they figments of the T cell's imagination?" Oh no, they're honest-to-goodness proteins all right. So they're recognized by the T-cells. My only point is that there's nothing viral about them. They may point to specific genes that code for them, but they have no proof that these genes are viral either. > >"Why don't you provide some cites that show "stressors" causing the > immunological peturbations that are seen in HIV infection?" [quoted text clipped - 9 lines] > and Vpu) are all figments of the rich imaginations of the geneticists. > There is nothing viral about them. Nothing viral about them? HIV Gag, Pol and Env show homology to all other retroviral Gag, Pol and Env proteins. They are clearly viral. Chris Noble snip >They are clearly viral. Heck. For Iconoclusterfuckwad, Just claiming the proteins are not viral does not mean his belief is correct. >"Heck. For Iconoclusterfuckwad, Just claiming the proteins are not viral does not mean his belief is correct." Still not getting it, eh? I also claim the moon is not made of cheese. If you are of the opinion that it actually is, it's up to you to prove it. And by the way, ain't-cha glad I'm back? >"HIV Gag, Pol and Env show homology to all other retroviral Gag, Pol and Env proteins. They are clearly viral." See what I mean? Only vague suggestions. The human genome is full of retroviral fossil DNA. Even if these stretches of DNA would yield RNA that codes for these proteins, that still would not mean that the proteins come from an exogenous virus that has invaded the body. > >"HIV Gag, Pol and Env show homology to all other retroviral Gag, Pol and > Env proteins. [quoted text clipped - 4 lines] > that codes for these proteins, that still would not mean that the proteins > come from an exogenous virus that has invaded the body. Iconoclaster, your news client automatically includes the attributions. This is done for two reasons, protocol and coherence. Any time you quote someone's material, you are supposed to identify its authorship. The other reason is that without that identification, it makes the thread difficult to follow. Doing so will also get me off your case. Like I said, your news client automatically includes the attributions. All you need to do is leave them there. How hard can that be? Sean McHugh . >"Like I said, your news client automatically includes the attributions. All you need to do is leave them there. How hard can that be? " Well, I hope this form will satisfy you. Usually, though, everyone knows very well to whom I'm replying. I think repeating another person's complete post before answering is a waste of badwidth; that's why I snip part of it. > >"Like I said, your news client automatically includes the attributions. > All you need to do is leave them there. How hard can that be? " > Well, I hope this form will satisfy you. Usually, though, everyone knows > very well to whom I'm replying. Count me as one who doesn't. > I think repeating another person's > complete post before answering is a waste of badwidth; that's why I snip > part of it. As do I, when I interject on a point. The few character attributions consume is small, especially for the information they impart. This was especially so with your recent posts. The posts that you were answering were no longer on Usenet. Without any name or context and after several days (not complaining about that), it is difficult to recall and follow multiple threads. Knowing the previous poster can provide some context. This is especially so if readers are also involved in different newsgroups, as I am. Retaining attributions for whom you are quoting, is not considered bad netiquette; the opposite is so. http://linux.sgms-centre.com/misc/netiquette.php ~ USENET and Mailing List posting netiquette ~ # QUOTE CORRECTLY. ~ When you reply to a message, almost all newsreaders and mail clients ~ will quote the text to which you're replying by adding a line or ~ phrase which attributes the original text to its author, and by ~ inserting a quotation mark (usually a ">" greater-than sign followed ~ by a space) on the left of the quoted text. ~ This serves two fundamental purposes: ~ 1. ~ Correct identification of the person to whom you're replying, ~ and ~ 2. ~ Correct attribution of the quoted text to the original author ~ and of the new text to you. Best Regards, Sean McHugh - >> >"HIV Gag, Pol and Env show homology to all other retroviral Gag, Pol and >> Env proteins. [quoted text clipped - 16 lines] > attributions. All you need to do is leave them there. How hard > can that be? The moron Iconoclaster uses a non-standard newsreader that is incapable of properly formatting Usenet postings. He is not snipping the attributions manually his inadequate software simple does not include them in his postings. Not only is he ignorant about HIV but is also an idiot when it comes to choosing software. Gary Stein >>"HIV Gag, Pol and Env show homology to all other retroviral Gag, Pol and >Env proteins. [quoted text clipped - 4 lines] >that codes for these proteins, that still would not mean that the proteins >come from an exogenous virus that has invaded the body. LOL. f.cking idiot. People have made this bullshit claim. Were it true, the gene sequences would be found in humans, regardless of HIV+ or HIV- status. They aren't. Indicating exogenous. Otherwise, you make this claim so it should be easy for you to provide the evidnece. You can't because it doesn't exist. Once again--you prove yourself to be so f.cking stupid I can only think of one man more of a dork than you. GW Bush. George M. Carter >"Were it true, the gene sequences would be found in humans, regardless of HIV+ or HIV- status." Of course. And do you have the nerve to tell me that anybody went to the trouble to set up two groups, one "HIV+" and one "HIV-", and look for genes that are present in one group and not in the other? Besides, that whole human genome project that has been reported on with such euphoric beating on the tom-toms is far from finished. There are still too many holes. But only those alleys are pursued that satisfy the paradigm and bring in money. ..would be found in humans... Indeed! It's hard to find something when you're not looking for it. >>"Were it true, the gene sequences would be found in humans, regardless of >HIV+ or HIV- status." > >Of course. And do you have the nerve to tell me that anybody went to the >trouble to set up two groups, one "HIV+" and one "HIV-", and look for >genes that are present in one group and not in the other? LOL...you don't KNOW this?? Which means you are saying all this crap about HIV not being exogenous based on...let's see--your fetid IMAGINATION! What a f.cking surprise. You're a dork. George M. Carter > >"Were it true, the gene sequences would be found in humans, regardless of > HIV+ or HIV- status." [quoted text clipped - 9 lines] > ..would be found in humans... Indeed! It's hard to find something when > you're not looking for it. Except people have looked. http://tinyurl.com/r4fme If HIV were an endogenous retrovirus you would be able to amplify complete HIV sequences from everybody using HIV PCR primers. Horwitz used low-stringency conditions so that even sequences with low similarity would be amplified. The best he could come up with were short sequences of around 20 bps that were highly repetive and contained little information. Chris Noble >Except people have looked. > >http://tinyurl.com/r4fme > >If HIV were an endogenous retrovirus you would be able to amplify >complete HIV sequences from everybody using HIV PCR primers. I was wondering if the Iconoclusterfuckwad would actually do research and look to see if this was the case. He didn't, of course. George M. Carter > >"HIV Gag, Pol and Env show homology to all other retroviral Gag, Pol and > Env proteins. [quoted text clipped - 4 lines] > that codes for these proteins, that still would not mean that the proteins > come from an exogenous virus that has invaded the body. The human genome does indeed contain retroviral DNA. We can tell they are retroviral because they show homology to gene sequences for exogenous retroviruses. None of the endogenous retroviruses show any significant sequence similarity to HIV. If HIV was an endogenous retrovirus then HIV would be detectable by DNA PCR in every single cell in every single human. It isn't. HIV is not endogenous. Chris Noble |
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