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I've posted this sort of thing in the "HIV/AIDS" debate thread, but I think this deserves its own thread:
QUOTE: Numerous reports have described modulatory effects of viruses or proteins of the viral envelopes on the arachidonic acid (AA) cascade. For example, Behera et al. [19] reported that respiratory syncytial virus (RSV) infection of a bronchial epithelial cell line leads to an up-regulation of the biosynthesis of LTs. These results were consistent with other findings showing that increased LT synthesis correlated with the presence of RSV particles in patients affected with pneumonia or bronchiolitis [20,21]. Exposure of monocytic cells to the HIV-1 glycoprotein gp120 induced the expression of cyclooxygenase and lipoxygenase pathway enzymes [22], and it was reported recently that the cytotoxic effect of gp120 on a neuroblastoma cell line involved activation of the AA cascade together with enhanced membrane lipid peroxidation [23]. We have described previously the capacity of EBV to prime monocytes for an increased synthesis of LTB4 and LTC4 through modulation of 5-LO activity [24]. In the present study, we show that exposure of PMN to EBV enhances levels of LTB4 biosynthesis upon stimulation with a second agonist through a mechanism implicating a direct stimulatory effect of EBV on cPLA2 phosphorylation (Ser-505) and a priming effect of the viral particles on the translocation of cPLA2 induced by neutrophil agonists. Since phagocytes play a crucial role in host defence against infectious agents, changes in the generation of proinflammatory mediators may be an important issue in the early events of viral infection... UNQUOTE.
Source: Clin Exp Immunol. 2001 December; 126(3): 494�?02.
On the internet:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1906243
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HIV replicates via Arachidonic Acid pathways.
http://gateway.nlm.nih.gov/MeetingAbstracts/102218160.html |
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| That study was over 10 years ago, they said: "Right now we are focusing on elucidating the mechanism of this regulation and identifying possible cellular factor(s) involved in this effect," but did their "focus" lead to anything? Basically, it's the excessive stressful biochemical activity that seems to be doing the damage, resulting in "disease," and because AA is so much more biochemically active than the natural Mead acid, it's easy for "researchers" to "implicate" AA in all kinds of problems. |
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| Well, youll notice that even mainstream medicine says that the primary factor behind HIV disease is the immune response to the virus. |
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This is what really irritates me about "orthodox" folks (and not just "HIV/AIDS" either), and that is that they don't state their position as a formal hypothesis, and so if you point out how it is impossible (what you think it is, in any case), with experimental refutation citations , they just change it and claim that you misunderstood something. This is what might be best phrased "sham science."
As to "HIV/AIDS," the idea (as best I can tell) is that particular cells are destroyed by "HIV" over time, though it's not clear if this destruction takes place gradually (which is silly, since the body has tremendous adaptive abilities) or after a long "latency" period. In the latter case, whatever brings "HIV" out of latency and makes it much more virulent than when the initial "infection" occurred should be considered the actual cause, and a great deal of research money should be spent on this, instead of worrying about "HIV." I'll bet if you ask ten different "AIDS experts" you will get several different explanations.
With regard to "inflammation," I may have seen some mention of it on an "orthodox" site, but nothing comes to mind, so if you could cite one that makes the claim that "HIV" causes a dangerous inflammatory response, I'd be interested to read how they phrase it. In the "early days," some called it "autoimmune deficiency syndrome," and of course that is laughable - why wouldn't you want to be "deficient" in autoimmune reactions, which can be very dangerous. One has to question human reason after doing scholarly research on "HIV/AIDS" and other "diseases," the "cholesterol hypothesis," and "essential fatty acids," and that's "just for starters."
What seems to happen is that in a "civilized" society, people learn from an early age to trust "experts" and many don't have time to do their own research, even if they wanted to, though "cognitive dissonance" seems to prevent many from even considering alternative possibilities. "Experts" learn from their teachers, and often what starts out as a working hypothesis becomes dogma over the course of a few generations of scientists. Moreover, in the biology-related fields, there seems to be a strong anti-scientific quality, in that many will say things like, "oh that's an old study" (even if it is on-point) or "it's all been settled, so there's no reason to waste time on that stuff." They don't seem to realize the importance of doing experiments to verify existing preconceptions, and this is especially egregious with something like "HIV/AIDS," where they have clearly failed, over and over again. It's too bad our society doesn't have a good concept for this phenomenon (i.e., not considering alternatives in the wake of repeated failure) - "group insanity" is one possibility, but then people will think of cults. |
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There is this:
http://jvi.asm.org/cgi/content/abstract/JVI.02228-07v1
And then there are small studies like this that suggest that supressing the immune system with corticosteroids will help:
http://www.aidsmap.com/en/news/A07AC512-407B-4743-8573-D1583E22C256.asp
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I took a look at your first citation, but there was only a short abstract (full text requires paid subscription). Here is one passage: "...these results suggest that activated CD4+ T cells from untreated HIV+ individuals are in a hyper-proliferative state that is modulated by Type I interferons. From these results, we propose a new model for CD4+ T cell depletion during chronic HIV-1 infection."
It's not clear (at least to me) why this should lead to a drastic drop in CD4+T cell levels, especially many years after "infection." And they don't talk specifically of inflammation either. I did my own search and this was the closest I found:
"...it is possible that HIV-associated inflammation promotes smoking-induced lung carcinogenesis..."
Source: http://dceg.cancer.gov/veb/research/hivaids
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