The ability of human immunodeficiency virus type-1 (HIV-I) to establish a p
ersistent infection is critically dependent on the cellular signals that re
gulate HIV-I replication within target cells. Tile balance between numerous
host factors that either enhance ol suppress viral infection determines th
e clinical outcome. Perturbation of the steady-state level of viral replica
tion can significantly influence the course and the speed at which the infe
ction develops into clinical disease. Activation signals delivered to T cel
ls by cytokines and antigen-presenting cells (APC), are key modulators of v
iral replication. Our laboratory seeks to decipher how HIV-I exploits T cel
l signaling mechanisms and host factors that regulate viral replication. El
ucidation of the molecular mechanisms by which cellular signals regulate th
e HIV-1 life cycle within target cells will significantly advance our under
standing of host-virus interactions.