Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat
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- Manabu Taura
- Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;
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- Eric Song
- Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;
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- Ya-Chi Ho
- Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520;
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- Akiko Iwasaki
- Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;
抄録
<jats:title>Significance</jats:title> <jats:p>Human immunodeficiency virus 1 (HIV-1) infection causes a life-long disease, due to the ability of the virus to integrate into the host genome and establish latent infection. While research has revealed a number of host restriction factors that block primary infection, much less is understood with regard to the host factors that promote or block reactivation of the integrated proviral HIV-1. In this study, we show that a member of the Apobec3A (apolipoprotein B MRNA editing enzyme catalytic subunit 3A) family, A3A, suppresses HIV-1 reactivation by recruiting chromatin-modifying enzymes to impose repressive marks around the long terminal repeat promoter region. Identification of host factors that control HIV-1 latency may provide clues for therapeutic interventions needed to remove the viral reservoir from the infected individual.</jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 116 (6), 2282-2289, 2019-01-22
Proceedings of the National Academy of Sciences