Host factors regulating post-integration latency of HIV.

A recent study has provided important clues towards the identity of the host genes that conspire to promote post-integration latency of human immunodeficiency virus (HIV). Various genes controlling transcription, histone deacetylation and proteasome-mediated protein degradation have emerged as potential players. If the desired, but difficult, goal of complete virus eradication in HIV-infected patients is ever to be realized, the latent reservoir of HIV proviruses must be cleared.

Nuclear export of Vpr is required for efficient replication of human immunodeficiency virus type 1 in tissue macrophages.

Retroviruses must gain access to the host cell nucleus for subsequent replication and viral propagation. Human immunodeficiency virus type 1 (HIV-1) and other primate lentiviruses are distinguished from the gammaretroviruses by their ability to infect nondividing cells such as macrophages, an important viral reservoir in vivo. Rather than requiring nuclear membrane breakdown during cell division, the HIV-1 preintegration complex (PIC) enters the nucleus by traversing the central aqueous channel of the limiting nuclear pore complex.