Mechanisms of infectivity and replication of HIV-1 and implications for therapy.

Human immunodeficiency virus type 1 (HIV-1), a retrovirus, is the etiologic agent of AIDS. Like all retroviruses, the viral genes are carried in the viral particle in the form of single-stranded RNA. Once inside a susceptible host cell, this RNA template is reverse-transcribed by virally supplied enzyme functions into a DNA copy, which becomes integrated permanently into the host's own genetic material. The genome of HIV-1, comprising approximately 10,000 bases, is much more complex than those of classic retroviruses, encoding a minimum of six gene products in addition to the gag, pol, and env genes characteristic of all retroviruses. These genes encode regulatory functions that act at diverse points in the virus life cycle. Together, they provide HIV-1 with an exceptional ability to modulate its replication depending on its host environment. This characteristic is reflected in the different stages presented by the disease and the diverse behaviors of the virus in different types of host cells. A greater understanding of the mechanics of this regulation and the factors that influence it may someday permit therapeutic intervention in the disease process that will halt virus replication and the progression of pathology in infected individuals.