HIV-1 Vpr counteracts HLTF-mediated restriction of HIV-1 infection in T cells.

ABSTRACT: Lentiviruses, including HIV-1, possess the ability to enter the nucleus through nuclear pore complexes and can infect interphase cells, including those actively replicating chromosomal DNA. Viral accessory proteins hijack host cell E3 enzymes to antagonize intrinsic defenses, and thereby provide a more permissive environment for virus replication. The HIV-1 Vpr accessory protein reprograms CRL4^DCAF1 E3 to antagonize select postreplication DNA repair enzymes and activates the DNA damage checkpoint in the G2 cell cycle phase. However, little is known about the roles played by these Vpr targets in HIV-1 replication. Here, using a sensitive pairwise replication competition assay, we show that Vpr endows HIV-1 with a strong replication advantage in activated primary CD4⁺ T

SUBMITTER: Yan J 

PROVIDER: S-EPMC6511057 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature