This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.We have developed a comparative infection model, in which SMs and RMs can be infected with the same SIV strain, enabling study of the divergent host responses that lead to BM suppression in RMs, but not in SMs. We will use this model to: 1) Identify the stages of hemapoiesis and T cell homeostasis suppressed by pathogenic SIV infection, 2) Identify candidate pathogenic mechanisms of BM suppression, and 3) Probe putative BM-suppressive pathways by specific interventions. Understanding HIV-induced BM suppression will be key for effective hematologic and immune reconstitution strategies. Our studies of SIV-infected sooty mangabeys (SMs), the natural reservoir host from which HIV-2 arose, demonstrate that SMs avoid CD4+ T cell loss and BM suppression despite high viremia. In contrast, SIV infection of the non-natural rhesus macaque (RM) host, recapitulates the BM suppression and lymphopenia seen in human AIDS.
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