Antagonism of SAMHD1 is actively maintained in natural infections of simian immunodeficiency virus.

ABSTRACT: Restriction factors are effectors of the innate immune response to viral pathogens that inhibit viral replication by operating as molecular barriers to steps of the viral life cycle. The restriction factor SAMHD1 blocks lentiviral reverse transcription in myeloid cells and resting CD4+ T cells. Many lineages of lentiviruses, including HIV-2 and other simian immunodeficiency viruses, encode accessory genes that serve to counteract host SAMHD1 restriction by causing degradation of the antiviral factor. The viral accessory protein Vpr is responsible for SAMHD1 degradation in some lineages of lentiviruses, whereas in others the related protein Vpx assumes this task. However, HIV-1 has no SAMHD1 degradation capability, leading to questions about the selective advantage of this activity. We use

SUBMITTER: Spragg CJ 

PROVIDER: S-EPMC3876209 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature