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10.1016/j.virol.2017.03.002

http://scihub22266oqcxt.onion/10.1016/j.virol.2017.03.002
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suck abstract from ncbi


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pmid28340355
      Virology 2017 ; 506 (ä): 34-44
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  • The Human Immunodeficiency Virus 1 ASP RNA promotes viral latency by recruiting the Polycomb Repressor Complex 2 and promoting nucleosome assembly #MMPMID28340355
  • Zapata JC ; Campilongo F ; Barclay RA ; DeMarino C ; Iglesias-Ussel MD ; Kashanchi F ; Romerio F
  • Virology 2017[Jun]; 506 (ä): 34-44 PMID28340355 show ga
  • Various epigenetic marks at the HIV-1 5'LTR suppress proviral expression and promote latency. Cellular antisense transcripts known as long noncoding RNAs (lncRNAs) recruit the polycomb repressor complex 2 (PRC2) to gene promoters, which catalyzes trimethylation of lysine 27 on histone H3 (H3K27me3), thus promoting nucleosome assembly and suppressing gene expression. We found that an HIV-1 antisense transcript expressed from the 3'LTR and encoding the antisense protein ASP promotes proviral latency. Expression of ASP RNA reduced HIV-1 replication in Jurkat cells. Moreover, ASP RNA expression promoted the establishment and maintenance of HIV-1 latency in Jurkat E4 cells. We show that this transcript interacts with and recruits PRC2 to the HIV-1 5'LTR, increasing accumulation of the suppressive epigenetic mark H3K27me3, while reducing RNA Polymerase II and thus proviral transcription. Altogether, our results suggest that the HIV-1 ASP transcript promotes epigenetic silencing of the HIV-1 5'LTR and proviral latency through the PRC2 pathway.
  • |*Virus Latency [MESH]
  • |Chromatin Assembly and Disassembly [MESH]
  • |Gene Expression Regulation, Viral [MESH]
  • |Gene Silencing [MESH]
  • |HIV Infections/genetics/metabolism/*virology [MESH]
  • |HIV Long Terminal Repeat [MESH]
  • |HIV-1/genetics/*physiology [MESH]
  • |Histones/metabolism [MESH]
  • |Host-Pathogen Interactions [MESH]
  • |Humans [MESH]
  • |Nucleosomes/genetics/*metabolism [MESH]
  • |Polycomb Repressive Complex 2/genetics/*metabolism [MESH]
  • |RNA, Antisense/genetics/*metabolism [MESH]


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