HTLV-I p30 inhibits multiple S phase entry checkpoints decreases cyclin E-CDK2 interactions and delays cell cycle progression

摘要

BackgroundHuman T-cell leukemia virus type I (HTLV-I) has efficiently adapted to its host and establishes a persistent infection characterized by low levels of viral gene expression and slow proliferation of HTLV-I infected cells over decades. We have previously found that HTLV-I p30 is a negative regulator of virus expression.