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Human immunodeficiency virus 1

ABSTRACT: HIV LTR terminus sequence

PROVIDER: PRJDB9357 | ENA |

REPOSITORIES: ENA

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Dataset's files

Source:

			Action	DRS
	DRR212764_1.fastq.gz	Fastqsanger.gz
	DRR212764_2.fastq.gz	Fastqsanger.gz
	DRR212765_1.fastq.gz	Fastqsanger.gz
	DRR212765_2.fastq.gz	Fastqsanger.gz
	DRR212766_1.fastq.gz	Fastqsanger.gz

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Project description:Schlafen-5 (SLFN5) is an interferon-induced protein of the Schlafen family which are involved in immune responses and oncogenesis. To date, little is known regarding its anti-HIV-1 function. Here, the authors report that overexpression of SLFN5 inhibits HIV-1 replication and reduces viral mRNA levels, whereas depletion of endogenous SLFN5 promotes HIV-1 replication. Moreover, they show that SLFN5 markedly decreases the transcriptional activity of HIV-1 long terminal repeat (LTR) via binding to two sequences in the U5-R region, which consequently represses the recruitment of RNA polymerase Ⅱ to the transcription initiation site. Mutagenesis studies show the importance of nuclear localization and the N-terminal 1-570 amino acids fragment in the inhibition of HIV-1. Further mechanistic studies demonstrate that SLFN5 interacts with components of the PRC2 complex, G9a and Histone H3, thereby promoting H3K27me2 and H3K27me3 modification leading to silencing HIV-1 transcription. In concert with this, they find that SLFN5 blocks the activation of latent HIV-1. Altogether, their findings demonstrate that SLFN5 is a transcriptional repressor of HIV-1 through epigenetic modulation and a potential determinant of HIV-1 latency.

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