Regulation of human immunodeficiency virus-1 latency and its reactivation.
Treatment of human immunodeficiency virus (HIV) infection with highly active antiretroviral therapy (HAART) has become highly effective. However the persistence of a small population of infected cells containing transcriptionally silent but re-activatable HIV proviruses prevents complete elimination of the infection. Here, we review recent progress in our understanding of the molecular mechanisms underlying HIV proviral latency and highlight experimental therapies designed to eliminate the latent population.
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Gladstone Institute of Virology and Immunology, University of California, San Francisco, USA.
D019380:Anti-HIV Agents / Q000627:therapeutic use; D023241:Antiretroviral Therapy, Highly Active / Q000379:methods; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000821:virology*; D002986:Clinical Trials as Topic; D019317:Evidence-Based Medicine; D015967:Gene Expression Regulation, Viral / Q000235:genetics; D016679:Genome, Viral; D015658:HIV Infections / Q000188:drug therapy / Q000235:genetics* / Q000276:immunology; D015497:HIV-1 / Q000187:drug effects / Q000235:genetics* / Q000276:immunology; D006801:Humans; D011533:Proviruses / Q000235:genetics; D014775:Virus Activation / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D016662:Virus Integration / Q000235:genetics; D017735:Virus Latency / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D054322:tat Gene Products, Human Immunodeficiency Virus / Q000235:genetics* / Q000276:immunology
D019380:Anti-HIV Agents; D054322:tat Gene Products, Human Immunodeficiency Virus