Intestinal Dysbiosis theory confirmed

The thread on Questioning AIDS mentioned in the previous post is not only about oxidative stress and that HAART adds more such damage, it refers also to a number of articles that lend considerable support to Tony Lance’s hypothesis of intestinal dysbiosis:  damage to the intestinal microflora destroys safeguards — in particular against fungal infections — and allows leakage of certain substances from gut to blood which in turn leads to testing “HIV-positive”.
Mainstream work seems increasingly to be edging toward accepting this view. For example:
“the gastrointestinal tract plays a critical role in the pathogenesis of acute HIV-1 . . . infections”
— Mehandru et al., Journal of Allergy and Clinical Immunology, 116 (2005) 419-22.
“The gastrointestinal pathology associated with HIV infection comprises significant enteropathy with increased levels of inflammation and decreased levels of mucosal repair and regeneration”
— Brenchley & Douek, Mucosal Immunology, 1 (2008) 23-30
“Why and how HIV makes people sick is highly debated. Recent evidence implicates heightened immune activation due to breakdown of the gastrointestinal barrier as a determining factor of lentiviral pathogenesis. . . . Translocation of microbial products from the gut, in turn, correlates with increased immune activation in chronic HIV infection and may further damage the immune system . . . . Maintaining a healthy GALT [gut-associated lymphoid tissue] may be the key to reducing the pathogenic potential of HIV”
— Hofer & Speck, Seminars in Immunopathology, 31 (2009) 257-66.
“Reducing the pathogenic potential of HIV” by maintaining a healthy GALT is quite like Montagnier’s assertion, captured in the House of Numbers film,     that a healthy immune system can stave off damage from “HIV” (some discussion here). In practical terms — no theorizing about causes — these mainstream statements mean and recommend  precisely the same as Lance does:
You have more chance of staying healthy, whether you are “HIV-positive” or “HIV”-negative, if you don’t do anything to harm your beneficial gut microflora. Be sensible in terms of lifestyle. Pay special attention to diet, and by all means use probiotics.

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The mainstream has been unable to identify specific mechanisms by which “HIV” is supposed to kill off the immune system. The currently favored idea seems to be that “HIV” somehow brings about chronic systemic immune activation:
“the increased CD4+ and CD8+ cell death and proliferation is a consequence of virus-induced immune activation, not virus-mediated killing”
— Douek, PRN Notebook, 10(#3) (2005) 9-12.
“Chronic activation of the immune system is a hallmark of progressive HIV infection and better predicts disease outcome than plasma viral load” [emphasis added]
— Brenchley et al., Nature Medicine, 12 (2006) 1365-71
“HIV infection is characterized by chronic immune system activation” (review article)
— Nixon & Landay, Current Opinion in HIV and AIDS, 5 (2010) 498-503.

But how does “HIV” produce that condition?
“circulating microbial products, probably derived from the gastrointestinal tract, are a cause of HIV-related systemic immune activation. . . . These data establish a mechanism for chronic immune activation in the context of a compromised gastrointestinal mucosal surface”
— Brenchley et al., Nature Medicine, 12 (2006) 1365-71
“Microbial translocation has been linked to systemic immune activation during human immunodeficiency virus (HIV) type 1 infection. Here, we show that an elevated level of microbial translocation . . . correlates with AIDS”
— Nowroozalizadeh et al., Journal of Infectious Diseases, 201 (2010) 1150-4.
So, again, precisely the Lance hypothesis: Damage to the gut’s protective functioning allows leakage into the blood of substances not normally there, producing chronic activation so long as the leakage persists. Eventually serious illness can result.

The salient difference between the Lance theory and the mainstream belief is this:
— If Lance is right, then damage to the gut microflora precedes whatever markers may be used to detect what is thought to be “HIV” or to diagnose what is considered “AIDS”.
— If the mainstream view is correct, then “HIV infection” causes the damage to the gut.

Now, according to Sankaran et al., Journal of Virology, 82 (2008) 538-45:
“HIV-induced pathogenesis in GALT [gut-associated lymphoid tissue] emerges at both the molecular and cellular levels prior to seroconversion in primary HIV infection, potentially setting the stage for disease progression by impairing the ability to control viral replication and repair and regenerate intestinal mucosal tissues. . . . deterioration of the intestinal mucosa may initiate rapidly following infection . . . . HIV-induced enteropathy is well established within the first few weeks of infection, potentially even prior to seroconversion” [emphases added].
The examined biopsy samples had been obtained “at 4 to 8 weeks following HIV infection”; 3 of the 4 patients were then HIV-negative, and the 4th seroconverted 2 days before the biopsy. “Four highly active antiretroviral therapy (HAART)-naive patients in the primary stage of HIV infection (4 to 8 weeks postinfection)” were studied. However, it is not explained how these individuals happened to be enrolled in this study and to be under observation even before seroconversion. The only mentioned reason for assuming “HIV infection” were “flu-like” symptoms, and at that time they tested HIV-negative. Cited earlier studies by the same authors give no more specific information about these individuals; the only clue is that the work seems to be associated with the Center for AIDS Research, Education and Services in Sacramento (CA): so perhaps gay men enroll who are concerned that they might be exposed to “HIV” and might at some time seroconvert?
At any rate, it seems permissible to doubt that the date of “HIV infection” could have been accurately known. But in any case this is immaterial for the present purpose. What is clear is that at some time prior to testing “HIV-positive”, these four individuals had experienced damage to the mucosal lymphoid tissue of the sort seen in “HIV disease” or “AIDS”.
That is precisely what Lance’s intestinal dysbiosis theory predicts.
The mainstream belief is that “HIV infection” immediately — albeit it not always! — produces “flu-like” symptoms, but that antibodies do not appear for several weeks. It seems at least equally plausible that damage to the gut’s immune system brings gut leakage and immune activation that immediately causes “flu-like” symptoms. After all, those symptoms — fever in particular — are the direct result of activation of the immune system as it responds to foreign presences.

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When Tony had first told me of his theory, it came as the answer to what had been for me the most puzzling aspect of the HIV/AIDS story, from the viewpoint of one who had already seen that “HIV” is not what it’s said to be. The puzzle was, why gay men tested “HIV-positive” at such high rates; even though many of them remained seemingly healthy; and why testing positive seemed maximally probable at ages in the thirties or early forties. The intestinal dysbiosis theory explains those: A certain degree of dysbiosis can produce a positive “HIV” test without causing significant ill health; but continuing damage to the gut microflora over a decade or two could bring ill health as well as testing “HIV” positive.

At the Oakland Conference, Tony described how he came to his theory. The abstract, slides, audio, and video of his talk are available at the Conference website.
(The YouTube version of Part 2 seems  to stop before the end of Tony’s talk.)
Watching that video, one must surely be impressed by the strength of character this man has displayed. He disclaims expertise in science, but Tony Lance has demonstrated the single most important feature of doing science properly: an unwavering determination to look at all the evidence and then to seek explanations for it.