The theme of this session was the discussion of emerging immunological dysfunctions in progressively HIV-infected humans and SIV-infected Asian macaques compared to naturally SIV-infected natural hosts. Dr. Ivona Pandrea (University of Pittsburg) discussed a novel therapeutic intervention to decrease microbial translocation-induced immune activation. She infected pigtail macaques with SIVagm and observed significant microbial translocation, cardiovascular disease, and immune activation in these animals. She then treated a subset of these SIVagm-infected pigtail macaques with rifaximin and sulfasalazine and noted that the treated animals had significantly reduced microbial translocation, inflammation and viral replication. Ms. Carol Vinton (NIAID, NIH) discussed cellular substrates for infection in natural hosts for SIV compared to nonnatural hosts for SIV. She found that lymph node resident and circulating peripheral blood CD4 T cell subsets were differentially targeted by SIV in naturally SIV-infected sooty mangabeys compared to progressively SIV-infected Asian macaques. Dr. Ann Chahroudi (Emory University) discussed how low numbers of target cells for SIV in young sooty mangabeys may limit vertical transmission in that natural host. She found very low frequencies of CCR5+ proliferating CD4 T cells in the mucosa of infant sooty mangabeys, potentially explaining the low incidence of vertical transmission in natural hosts for SIV. Dr. Gilad Doitsh (Gladstone Institute) discussed how depletion of CD4 T cells in HIV-infected individuals may be, in part, attributed to activation of infected CD4 T cells. He used in vitro infection of lymph node cultures and showed that the majority of HIV-infected cells are abortively HIV infected and that their death was attributed to activation-induced pyroptosis instead of direct virus-mediated killing and that this activation-induced death could be blocked by the FDA approved drug glimepiride. Mr. Feras Al-Ghazawi (University of Ottowa) discussed how IL-7 signalling may lead to a feedback inhibition of future IL-7 signals. He found IL-7 induced expression of SOCS1-3 and significant down-regulation of the IL-7 receptor CD127. He then showed by coimmunoprecipitation that SOCS proteins may lead directly to down-regulation of CD127.