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Chromatin, gene silencing and HIV latency

Hoi Ping Mok, +1 more
- 23 Nov 2007 - 
- Vol. 8, Iss: 11, pp 228-228
TLDR
The relationship of viral latency to gene-silencing mechanisms is reviewed, and it is shown that at least two gene- silencing mechanisms are used against the human immuno-deficiency virus.
Abstract
One of the cellular defenses against virus infection is the silencing of viral gene expression. There is evidence that at least two gene-silencing mechanisms are used against the human immuno-deficiency virus (HIV). Paradoxically, this cellular defense mechanism contributes to viral latency and persistence, and we review here the relationship of viral latency to gene-silencing mechanisms.

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Integration site selection by retroviruses and transposable elements in eukaryotes

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An HIV-encoded antisense long noncoding RNA epigenetically regulates viral transcription.

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Snapshots: chromatin control of viral infection.

TL;DR: This review represents a compilation of conceptual snapshots of the dynamic interplay of viruses with the chromatin environment, focusing on chromatin dynamics during infection, viral circumvention of cellular chromatin repression, chromatin organization of large DNA viruses, tethering and persistence, and control of viral latency-reactivation cycles.
References
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Journal ArticleDOI

MicroRNAs: Genomics, Biogenesis, Mechanism, and Function

TL;DR: Although they escaped notice until relatively recently, miRNAs comprise one of the more abundant classes of gene regulatory molecules in multicellular organisms and likely influence the output of many protein-coding genes.
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Alu repeats and human genomic diversity

TL;DR: During the past 65 million years, Alu elements have propagated to more than one million copies in primate genomes, which has resulted in the generation of a series of Alu subfamilies of different ages.
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Retroviral DNA integration: ASLV, HIV, and MLV show distinct target site preferences.

TL;DR: Each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection.
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HIV reproducibly establishes a latent infection after acute infection of T cells in vitro

TL;DR: Direct sequencing of integration sites demonstrated that latent clones frequently contain HIV integrated in or close to alphoid repeat elements in heterochromatin, demonstrating that HIV can reproducibly establish a latent infection as a consequence of integration in or near heterochROMatin.
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