Below I will attempt to show you the strange trend in some of the "sciences" these days which involves placing a higher value on assumptions and models than on obvious, demonstrable, direct effects of molecules on cells or other molecules. First, let's take a look at the following abstract of a study. Do not worry if you don't understand much of it, because I will explain it after you read it, and remember that you can always post a question in the messages section if you have one.

Proc Natl Acad Sci U S A. 1986 May; 83(10): 3487�?490. Prostaglandin E2, a seminal constituent, facilitates the replication of acquired immune deficiency syndrome virus in vitro. S Kuno, R Ueno, O Hayaishi, H Nakashima, S Harada, and N Yamamoto Acquired immune deficiency syndrome (AIDS)-associated virus is thought to be transmitted effectively through semen during sexual activities from male to male or from male to female. Prostaglandin (PG) E2 is one of the immunosuppressive compounds present in high concentrations in human semen. We, therefore, investigated direct effects of PGE2 and other PGs on AIDS-associated virus infection and replication in vitro. First, type III human T-lymphotropic virus (HTLV-III) was used to infect a T-cell line (MT-4) in culture. PGE2 (10 nM to 10 microM) added to the culture medium enhanced the production of infectious virus in a dose-dependent fashion. In the presence of 5 microM PGE2, 2.5-fold more virus were released from the infected MT-4 cells as compared to untreated control cells on day 3 after infection. Second, when we used an HTLV-III continuous-producer cell line (Molt-4/HTLV-III), PGE2 and PGD2 added to the culture medium increased the number of viruses released from Molt-4/HTLV-III cells. Other PGs such as PGF2 alpha and 13,14-dihydro-15-keto PGE2 did not affect the replication of HTLV-III in this system. These results indicate that some PGs including seminal PGs enhance the AIDS-associated virus replication in vitro. We propose that PGE2 in human semen might directly facilitate the infection of AIDS-associated virus and cause the efficient transmission of the virus during sexual activities.

This abstract presents a good example of how one needs to “read between the lines�?in studies. In this one, we are told about “thoughts,�?yet then they say that something “enhanced the production of infectious virus.�? Do you see the ridiculous inconsistency here? If it was never determined that there was a truly infectious and deadly virus transmitted, how was it so easy to determine that “production of infectious virus�?was enhanced? The question to ask here is, what exactly was enhanced? We know that “markers�?must have been used, not actual “HI�?virus, since nobody has done that to date. Which markers were they? Were they antibodies or protein fragments? They start with assumptions, use markers that have never been demonstrated to be consistent only with the “HIV/AIDS�?notion, and then they propose that PGE2 is aiding viral “infection,�?when an alternative hypothesis makes more sense, considering what is known about the deleterious effects of AA metabolites. By far the best explanation for what their results is that the PGE2 caused cellular damage, leading to reverse transcriptase activity. As the Perth Group note:

“In 1983 Montagnier claimed he had isolated HIV because he could pass it to cultures containing lymphocytes originating from a healthy blood donor and umbilical cord. He made the same claim at the beginning of Djamel Tahi's interview, "we did isolation because we "passed on" the virus".9 By “passing�?he meant detection of reverse transcription (RT) in the culture which contained lymphocytes from his patient, BRU, and in the co-cultures with lymphocytes or supernatants from the BRU culture and lymphocytes from a healthy donor or umbilical cord. He claimed the detection of RT activity was proof for isolation because this activity was "truly specific of retroviruses". However, after repeated questioning he admitted that reverse transcriptive activity is not specific to retroviruses and thus, indirectly, that he did not isolate HIV. In addition, detection of an enzymatic activity, even if specific to retroviruses, is not evidence for isolation. For example, the measurement of cardiac or liver enzymes in cases of myocardial infarction or hepatitis respectively cannot be construed as "isolation" of the heart or liver.�

Source: http://www.rethinking.org/bmj/response_49374.html

Note that one could a control experiment, but the problem is that when they say they used “infected cells,�?we don’t know what they mean, because the “HI�?virus was never isolated and demonstrated to do specific damage to specific cells. It’s all assumptions and speculation to this day, more than 20 years after the “AIDS epidemic�?began, even though very little money, relatively-speaking, could decide the matter once and for all (because the technology is available and not extremely difficult to apply in this matter).

Note also that they talk about the “direct effects�?of PGE2. We know that the PGE2 is enhancing something that appears to lead to health problems, but they never stop to think that the PGE2 might be the biggest problem. Since the PGE2 molecule can be isolated and at least some if its deleterious effects are known, and since it is also known that semen (of those with AA overload) is rich in semen, and moreover since receptive anal intercourse is correlated with “AIDS,�?there is no need for speculating about a virus that has not been isolated (despite at least somewhat competent attempts to do so), for which a vaccination has not been developed (despite repeated promises that this would occur “in the near future�?, and for which no detectable direct damage has ever been observed.

Now here is a passage from another abstract concerning PGE2:

Eur J Immunol. 1995 Jan;25(1):59-63. Differential modulation of T helper type 1 (Th1) and T helper type 2 (Th2) cytokine secretion by prostaglandin E2 critically depends on interleukin-2. Hilkens CM, Vermeulen H, van Neerven RJ, Snijdewint FG, Wierenga EA, Kapsenberg ML. Department of Cell Biology and Histology, University of Amsterdam, The Netherlands. Prostaglandin E2 (PGE2) favors T helper type 2 (Th2)-like cytokine secretion profiles in murine and human CD4+ T cells by inhibiting the production of the Th1-associated cytokines interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) and up-regulating the production of the Th2-associated cytokines IL-4 and IL-5 in a dose-dependent way....

This is what happens in many cases of "HIV/AIDS," that is, a shift from Th1 to Th2, less IL-2, etc. Note that one can't say anything definitive about "HIV/AIDS," since the the definition varies from one region or nation to another, and that the definition, even within the USA, has changed over the years. And now, in fact, Walter Reed medical facitily does not regard Kaposi's Sarcoma as an "AIDS defining disease," whereas other major US medical institutions do. Moreover, if a woman has cervical cancer and is "HIV positive," and dies of the cancer, she is counted as an "HIV/AIDS" death. I don't know if such a patient would have low IL-2 levels, a Th1 to Th2 shift, etc., and to me this is a ridiculous situation the "experts" have created, basically making it impossible to connect what is occurring at the molecular level with actual symptoms and "diseases," which for me is what should be regarded as the highest level of "medical" and "biological" understanding. Oh what a tangled web they have woven is about all the intelligent, well-read observer can say abou what they have done to this point.

If I were in charge I would put great resources into determining what is going on in the bodies of "AIDS" patients and just about everyone else who is said to be "diseased" in some way or another, in order to determine what molecules were involved and what damage was being done. Another important molecule that is enhanced in "HIV/AIDS" is TNF-alpha, and once again, the direct molecular-level evidence is present and abundant, for example:

Br J Pharmacol. 2000 Aug;130(7):1655-63. FK506 potently inhibits T cell activation induced TNF-alpha and IL-1beta production in vitro by human peripheral blood mononuclear cells. Sakuma S, Kato Y, Nishigaki F, Sasakawa T, Magari K, Miyata S, Ohkubo Y, Goto T. Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd, 2-1-6, Kashima, Yodogawa-ku, Osaka 532-8514, Japan. The aim of this study was to elucidate the in vitro inhibitory potency of FK506 on production of the inflammatory cytokines, tumour necrosis factor (TNF)-alpha and interleukin (IL)-1beta, with a view to assessing this immunosuppressive agent as a potential anti-rheumatic drug... These results strongly suggest that FK506 may be most effective to specifically prevent T cell activation mediated inflammatory cytokine production in a clinical setting.

This substance, FK506, is apparently being considered as a "medication" in RA, one can infer. Note that those with RA often test "positive" for "HIV infection." What is occurring at the molecular level is similar in both RA and "HIV/AIDS," though in RA the damage may be more specific. There is a clear progression of events: first, there is an inflammatory response that is too potent, resulting in damage and dysfunction, then the damaged cells and tissues can lead to other problems (such as "opportunistic infections," "wasting syndromes," "dementia," etc.) depending upon the exact stressors involved, which will vary from one individual to another (and inviduals vary in terms of resistance, which varies from one tissue, organ, or cell type to another). If one does not "nip" the problem "in the bud," things become very complicated, and the people in charge have shown no capacity for dealing effectively with this complexity. Instead, if the stressors are removed and if people were to rid their bodies of arachidonic acid (which would mean no PGE2 production and no enhancement of the infammatory process in general), the molecular-levels events will not occur or will be greatly attenuated, leading to much less "disease" and much milder symptoms in those who are afflicted with the "disease."