title: The multifactorial nature of HIV-1 latency.
abstract: HIV-1 can avoid host immune responses and antiretroviral drugs through the latent infection of resting memory CD4(+) T cells. Recently, latent viral genomes have been shown to reside within the introns of active host genes. Therefore, latency is not simply due to an inaccessibility of the integrated proviruses to the transcriptional machinery. Rather, latency might result from insufficient nuclear levels of the crucial activation-dependent host transcription factors required to overcome the transcriptional interference that is an automatic consequence of the nature of HIV-1 integration sites. In addition, resting cells lack sufficient levels of HIV-1 Tat and Tat-associated activation-dependent host factors that are necessary for processive transcription. Defects at consecutive steps of transcriptional initiation and elongation enable HIV-1 to remain hidden within resting CD4(+) T cells.
authors.affiliation: Johns Hopkins University School of Medicine, 879 BRB, 733N, Baltimore, MD 21205, USA.
authors.forename: Kara
authors.initials: K
authors.lastname: Lassen
authors.forename: Yefei
authors.initials: Y
authors.lastname: Han
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhou
authors.forename: Janet
authors.initials: J
authors.lastname: Siliciano
authors.forename: Robert F
authors.initials: RF
authors.lastname: Siliciano
mesh_terms: D015496:CD4-Positive T-Lymphocytes / Q000821:virology; D015967:Gene Expression Regulation, Viral; D015658:HIV Infections / Q000821:virology*; D015497:HIV-1 / Q000235:genetics* / Q000502:physiology; D006801:Humans; D011533:Proviruses / Q000235:genetics / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics* / Q000502:physiology; D014158:Transcription, Genetic; D016662:Virus Integration / Q000235:genetics*; D017735:Virus Latency / Q000235:genetics* / Q000502:physiology
chemical_list: D014157:Transcription Factors