Immune activation, HIV persistence, and the cure.
HIV infection is characterized by persistent immune activation, even in the context of suppressive antiretroviral therapy. This persistent activation, which appears to be fueled by microbial translocation from the gut resulting from HIV-related damage, is associated with deficits in immune function that in turn contribute to persistent activation. The presence of latent HIV reservoirs in lymphoid tissues also provokes immune activation in the context of immune suppression, resulting in expansion of the viral reservoir and potential viral replication, even with suppressive antiretroviral therapy. Therapeutic strategies are being devised to reduce persistent immune activation and limit the size of the HIV reservoir. This article summarizes a presentation by Daniel C. Douek, MD, PhD, at the IAS-USA continuing education program held in San Francisco, California, in March 2013.
National Institutes of Health, Bethesda, MD, USA.
Daniel C
DC
Douek
D019380:Anti-HIV Agents / Q000627:therapeutic use*; D018988:Bacterial Translocation / Q000276:immunology; D041981:Gastrointestinal Tract / Q000276:immunology* / Q000382:microbiology / Q000821:virology; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology* / Q000821:virology; D015497:HIV-1 / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology*; D011760:Pyrrolidinones / Q000627:therapeutic use; D000068898:Raltegravir Potassium; D019562:Viral Load; D017735:Virus Latency; D014779:Virus Replication
D019380:Anti-HIV Agents; D011760:Pyrrolidinones; D000068898:Raltegravir Potassium