Regulation of HIV-1 gene transcription: from lymphocytes to microglial cells.
Transcription is a crucial step for human immunodeficiency virus type 1 (HIV-1) expression in all infected host cells, from T lymphocytes, thymocytes, monocytes, macrophages, and dendritic cells in the immune system up to microglial cells in the central nervous system. To maximize its replication, HIV-1 adapts transcription of its integrated proviral genome by ideally exploiting the specific cellular environment and by forcing cellular stimulatory events and impairing transcriptional inhibition. Multiple cell type-specific interplays between cellular and viral factors perform the challenge for the virus to leave latency and actively replicate in a great diversity of cells, despite the variability of its long terminal repeat region in different HIV strains. Knowledge about the molecular mechanisms underlying transcriptional regulatory events helps in the search for therapeutic agents that target the step of transcription in anti-HIV strategies.
Rohr
Olivier
O
Institut National de la Santé Recherche Médicale Unité, Strasbourg, France.
Marban
Céline
C
Aunis
Dominique
D
Schaeffer
Evelyne
E
D015496:CD4-Positive T-Lymphocytes / Q000821:virology; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D015967:Gene Expression Regulation, Viral; D016325:HIV Long Terminal Repeat / Q000235:genetics; D015497:HIV-1 / Q000235:genetics*; D006801:Humans; D008214:Lymphocytes / Q000821:virology*; D017628:Microglia / Q000821:virology*; D008954:Models, Biological; D009000:Monocytes / Q000821:virology; D016328:NF-kappa B / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D014158:Transcription, Genetic
D017362:Cyclic AMP Response Element-Binding Protein; D016328:NF-kappa B; D014157:Transcription Factors