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- W2911795872 abstract "Significance 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." @default.
- W2911795872 created "2019-02-21" @default.
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- W2911795872 date "2019-01-22" @default.
- W2911795872 modified "2023-09-28" @default.
- W2911795872 title "Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat" @default.
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- W2911795872 doi "https://doi.org/10.1073/pnas.1819386116" @default.
- W2911795872 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6369738" @default.
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