Our key target for re-mobilization of HIV-infected cells is S1PR1receptor-dependent egress of T cells from lymph nodes.  Our research identified HIV-Nef to inactivate S1PR1 functions.  We aim to interfere with Nef signaling by identifying the Nef-PAk2 interface.  

Successful eradication of HIV will depend on a combined therapeutic strategy including  eliminating viral latency  and reservoir retention.