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.The ability of human immunodeficiency virus type-1 (HIV-1) to establish a persistent infection is critically dependent on the cellular signals that regulate HIV-1 replication within target host cells. We propose to identify the activation signals and the signaling mechanisms that are required to render resting T cells susceptible to productive infection. We postulate that the antigenic-independent signals relayed from cytokines and the antigen-presenting cellsactivate bystander resting T cells which in turn is exploited by HIV-1 to infect these target cells. This hypothesis may explain how high viral replication and the T cell turnover is sustained throughout the infection. By pursuing these studies we expect to gain insights into how HIV-1 exploits host's antigen-independent signaling machinery to infect the target cells and the mechanisms of viral spread in vivo.
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