ABSTRACT
Department of Medicinal Chemistry ,+ Department of Biological Chemistry,s Merck Research Laboratories, P. 0. Box4, WP26-410, West Point, Pennsylvania 19486
INTRODUCTION
Hum an immunodeficiency vims (HIV) has been identified as the causative agent of acquired immunodeficiency syndrome (AIDS) in humans. Infection of monocytes expressing surface CD4 receptors by the vims eventually produces profound defects in cell m ediated immunity. Over time infection leads to severe depletion of CD4+ T-lymphocytes resulting in opportunistic infections, neurologic and neoplastic disease, and ultimately death. Although the precise basis of HIV pathogenicity is no t understood, the primary strategy for treating this disease relies on blocking viral replication. Analysis of the molecular events critical to vims replication has identified a num ber of possibilities to achieve this goal. Among those, blockade of the virally encoded protease (HIV PR) has become a major target in the quest for an effective therapeutic agent against HIV infection.
