HIV-1 replication is controlled at the level of T cell activation and proviral integration.

摘要: During progression of the Acquired Immune Deficiency Syndrome (AIDS), human immunodeficiency virus type 1 (HIV-1) is harbored in CD4+ T cells, which act as primary reservoir for virus. In vitro, HIV-1 requires activated cells a productive infection; however, vivo, number circulating state that are potential targets infection low. We have investigated ability to infect resting and consequences such an infection. cell activation was not required viral DNA unable integrate maintained extrachromosomally. Subsequent allowed integration extrachromosomal forms led life cycle. Extrachromosomal were found persist several weeks after and, following activation, these their template infectious Several lines evidence, including temporal analysis replication integrase deletion mutant, indicated extra-chromosomal genomes transcriptionally active. These results compatible with model whereby can non-productive until subsequent antigen-induced or mitogen-induced release. Thus agents induce may control rate spread during AIDS progression.