Novel regulation of HIV-1 replication and pathogenicity: Rev inhibition of integration.

ABSTRACT: Following fusion of the human immunodeficiency virus type-1 (HIV-1) with host cells' membrane and reverse transcription of the viral RNA, the resulted cDNA is integrated into the host genome by the viral integrase enzyme (IN). Quantitative estimations have revealed that only 1-2 copies are integrated per infected cell, although many copies of the viral RNA are reverse-transcribed. The molecular mechanism that restricts the integration degree has not, so far, been elucidated. Following integration, expressed partially spliced and unspliced transcripts are exported from the nuclei by the viral Rev protein. Here, we show that in virally infected cells, the Rev interacts with the IN forming a Rev-IN complex and consequently limits the number of integration events. Disruption of the Rev-IN comp

SUBMITTER: Levin A 

PROVIDER: S-EPMC2777023 | biostudies-literature | 2009 Dec

REPOSITORIES: biostudies-literature