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    • Guest Pyroboy74
      By Guest Pyroboy74
      Well, since I have decided to stop taking my meds and begin my path to AIDS and all other STDs, what better way to start than by going to the bathhouse? If any of you gentlemen happen to be in Dallas, I would gladly take your load(s) before/during/after my breeding at Midtowne. I'm hoping that there will be a decent amount of people tonight, the only problem with working the weekend is that I can't go take every load on the busiest nights. 
       
      Well, wish me luck! If you have an STD to add, or just want to slip a load inside, feel free to message me. I am hoping to beat my record of 8 loads in a day (sadly these won't all be poz like those were)
    • By jeff238
      Found this interesting article from THE SCIENTIST magazine. published Dec, 2013.
      I never heard of these studies and their findings before now.

      They suggest that there may be an accessible and inexpensive treatment to HIV caused CD4 T cell
      mass death.

      A few excerpts, since the article is quite long.

      "...HIV leads to AIDS primarily because the virus destroys essential immune cells called CD4 T cells,
      but precisely how these cells are killed has not been clear. Two papers published simultaneously
      today (December 19) in Nature and Science reveal the molecular mechanisms that cause the death of
      most CD4 T cells in lymphoid tissues, the main reservoir for such cells, during infection.

      ...The death of CD4 T cells during HIV infection has generally been attributed to plain old apoptosis,
      or programmed cell death. Problem is, most studies have focused on active cells in the blood, which
      are “productively infected” by HIV, meaning that the virus has integrated with host-cell genome and
      can make copies of itself. In a 2010 study, Greene and his colleagues showed that 95 percent of
      CD4 T cells in lymphoid tissue, by contrast, are bystander cells that are “abortively infected”—the
      virus penetrates but can’t integrate or replicate. To better understand HIV pathogenesis, Greene
      sought to figure out how this particular population of immune cells dies during HIV infection.

      ...For the study published in Nature, the team looked at human spleen and tonsil tissue cultured in
      the lab and spiked with HIV. The researchers found that when the virus productively infects the few
      permissive CD4 T cells present, death occurs through apoptosis mediated by an enzyme called caspase-3.
      But when HIV abortively infects nonpermissive CD4 T cells, death occurs by pyroptosis, which depends
      on the activation of caspase-1. It turns out that the vast majority—roughly 95 percent—of CD4 T cell
      death in lymphoid tissues is driven by caspase-1-mediated pyroptosis.

      ...In bacterial infection, the release of inflammatory signals is thought to promote clearance by
      attracting more immune cells to help. In a pathogenic inflammation scenario like HIV infection,
      however, the strategy backfires. Instead of clearing the infection, proinflammatory signals released
      by pyroptosis attract more cells into the infected tissue to die and, in turn, produce more
      inflammation. “The cavalry come riding in and fall victim to this same form of fiery cell death,
      turning their rifles on themselves,” says Greene.

      ...The discoveries could help researchers come up with new treatments that restrain the hosts’
      destructive response to HIV rather than the virus itself. The authors showed in the Nature study
      that an existing caspase-1 inhibitor—a drug already shown to be safe in humans—suppressed CD4 T-cell
      death and inflammation in cell culture. They are now planning a Phase II clinical trial to test its
      capacity to block pyroptosis in HIV-infected patients.

       Fauci said such an approach would not replace antiretrovirals (ARVs), which suppress HIV replication
      and halt disease progression. But it could be used in combination in people who are dealing with
      highly resistant HIV strains to reduce the destruction of CD4 T cells and inflammation. “One of the
      things about blocking the host response is that it's very difficult for the virus to mutate to
      counteract it,” added Fauci.

      Greene pointed out that a caspase-1 inhibitor might also provide a bridge therapy for the millions
      of people without access to ARVs. He added that such drugs might even prevent expansion of the
      reservoir of latent virus that lies low in memory CD4 T cells, which has so far precluded a cure
      for HIV/AIDS.

      The dysregulated action of cytokines during chronic inflammation might stimulate the homeostatic
      proliferation of memory CD4 T cells. “If we get rid of chronic inflammation, will we stop the
      homeostatic proliferation and degrade the latent reservoir?” asked Greene. “That’s something we can
      test. If it does, caspase-1 inhibitors might—and I emphasize might—become a component of a curative
      cocktail.”

        So naturally I looked to see what caspase inhibitor they might be talking about. There is really only
      one. CrmA, derived from the cow pox virus, inhibits caspase 1,8,10.

      All very interesting stuff. A study, just using the anti-inflamitory caspase inhibitor could actually
      arrest the progression of HIV infection. The person would still be a carrier, but would show little to
      no symptoms, by way of letting productively infected cells (5%) die, while saving the other 95% from
      pyroptosis. At least that's my take on it.
       
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