Published online before print August 11, 2003
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Institut National de la Santé et de la Recherche Médicale Unité 575, Strasbourg, France
1Correspondence: Unité 575 INSERM, 5 rue Blaise Pascal, 67084 Strasbourg, France. E-mail: schaeffer{at}neurochem.u-strasbg.fr
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.
Key Words: cellular specificity LTR Tat acetylation monocytes
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