title: Suppression of microRNA-silencing pathway by HIV-1 during virus replication.
abstract: MicroRNAs (miRNAs) are single-stranded noncoding RNAs of 19 to 25 nucleotides that function as gene regulators and as a host cell defense against both RNA and DNA viruses. We provide evidence for a physiological role of the miRNA-silencing machinery in controlling HIV-1 replication. Type III RNAses Dicer and Drosha, responsible for miRNA processing, inhibited virus replication both in peripheral blood mononuclear cells from HIV-1-infected donors and in latently infected cells. In turn, HIV-1 actively suppressed the expression of the polycistronic miRNA cluster miR-17/92. This suppression was found to be required for efficient viral replication and was dependent on the histone acetyltransferase Tat cofactor PCAF. Our results highlight the involvement of the miRNA-silencing pathway in HIV-1 replication and latency.
authors.affiliation: Laboratoire de Virologie Moléculaire, Institut de Génétique Humaine, Montpellier, France.
authors.forename: Robinson
authors.initials: R
authors.lastname: Triboulet
authors.forename: Bernard
authors.initials: B
authors.lastname: Mari
authors.forename: Yea-Lih
authors.initials: YL
authors.lastname: Lin
authors.forename: Christine
authors.initials: C
authors.lastname: Chable-Bessia
authors.forename: Yamina
authors.initials: Y
authors.lastname: Bennasser
authors.forename: Kevin
authors.initials: K
authors.lastname: Lebrigand
authors.forename: Bruno
authors.initials: B
authors.lastname: Cardinaud
authors.forename: Thomas
authors.initials: T
authors.lastname: Maurin
authors.forename: Pascal
authors.initials: P
authors.lastname: Barbry
authors.forename: Vincent
authors.initials: V
authors.lastname: Baillat
authors.forename: Jacques
authors.initials: J
authors.lastname: Reynes
authors.forename: Pierre
authors.initials: P
authors.lastname: Corbeau
authors.forename: Kuan-Teh
authors.initials: KT
authors.lastname: Jeang
authors.forename: Monsef
authors.initials: M
authors.lastname: Benkirane
mesh_terms: D020413:3' Untranslated Regions; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D005786:Gene Expression Regulation; D015696:Gene Products, tat / Q000378:metabolism; D015497:HIV-1 / Q000235:genetics / Q000502:physiology*; D006367:HeLa Cells; D051548:Histone Acetyltransferases / Q000235:genetics / Q000378:metabolism; D006801:Humans; D019169:Jurkat Cells; D007963:Leukocytes, Mononuclear / Q000201:enzymology / Q000821:virology*; D035683:MicroRNAs / Q000235:genetics*; D020411:Oligonucleotide Array Sequence Analysis; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics; D043244:Ribonuclease III / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014162:Transfection; D017735:Virus Latency; D014779:Virus Replication; D050880:p300-CBP Transcription Factors; D054322:tat Gene Products, Human Immunodeficiency Virus; D000099224:p300-CBP-Associated Factor
chemical_list: D020413:3' Untranslated Regions; D018797:Cell Cycle Proteins; D015696:Gene Products, tat; D051548:Histone Acetyltransferases; D035683:MicroRNAs; D034741:RNA, Small Interfering; D043244:Ribonuclease III; D014157:Transcription Factors; D050880:p300-CBP Transcription Factors; D054322:tat Gene Products, Human Immunodeficiency Virus; D000099224:p300-CBP-Associated Factor; C517918:DROSHA protein, human