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MicroRNA Regulation of Human Herpesvirus Latency

Herpesviruses are ubiquitous human pathogens. After productive (lytic) infection, all human herpesviruses are able to establish life-long latent infection and reactivate from it. Latent infection entails suppression of viral replication, maintenance of the viral genome in infected cells, and the abi...

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Detalles Bibliográficos
Autores principales: Chen, Siyu, Deng, Yue, Pan, Dongli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9231095/
https://www.ncbi.nlm.nih.gov/pubmed/35746686
http://dx.doi.org/10.3390/v14061215
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author Chen, Siyu
Deng, Yue
Pan, Dongli
author_facet Chen, Siyu
Deng, Yue
Pan, Dongli
author_sort Chen, Siyu
collection PubMed
description Herpesviruses are ubiquitous human pathogens. After productive (lytic) infection, all human herpesviruses are able to establish life-long latent infection and reactivate from it. Latent infection entails suppression of viral replication, maintenance of the viral genome in infected cells, and the ability to reactivate. Most human herpesviruses encode microRNAs (miRNAs) that regulate these processes during latency. Meanwhile, cellular miRNAs are hijacked by herpesviruses to participate in these processes. The viral or cellular miRNAs either directly target viral transcripts or indirectly affect viral infection through host pathways. These findings shed light on the molecular determinants that control the lytic-latent switch and may lead to novel therapeutics targeting latent infection. We discuss the multiple mechanisms by which miRNAs regulate herpesvirus latency, focusing on the patterns in these mechanisms.
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spelling pubmed-92310952022-06-25 MicroRNA Regulation of Human Herpesvirus Latency Chen, Siyu Deng, Yue Pan, Dongli Viruses Review Herpesviruses are ubiquitous human pathogens. After productive (lytic) infection, all human herpesviruses are able to establish life-long latent infection and reactivate from it. Latent infection entails suppression of viral replication, maintenance of the viral genome in infected cells, and the ability to reactivate. Most human herpesviruses encode microRNAs (miRNAs) that regulate these processes during latency. Meanwhile, cellular miRNAs are hijacked by herpesviruses to participate in these processes. The viral or cellular miRNAs either directly target viral transcripts or indirectly affect viral infection through host pathways. These findings shed light on the molecular determinants that control the lytic-latent switch and may lead to novel therapeutics targeting latent infection. We discuss the multiple mechanisms by which miRNAs regulate herpesvirus latency, focusing on the patterns in these mechanisms. MDPI 2022-06-02 /pmc/articles/PMC9231095/ /pubmed/35746686 http://dx.doi.org/10.3390/v14061215 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Chen, Siyu
Deng, Yue
Pan, Dongli
MicroRNA Regulation of Human Herpesvirus Latency
title MicroRNA Regulation of Human Herpesvirus Latency
title_full MicroRNA Regulation of Human Herpesvirus Latency
title_fullStr MicroRNA Regulation of Human Herpesvirus Latency
title_full_unstemmed MicroRNA Regulation of Human Herpesvirus Latency
title_short MicroRNA Regulation of Human Herpesvirus Latency
title_sort microrna regulation of human herpesvirus latency
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9231095/
https://www.ncbi.nlm.nih.gov/pubmed/35746686
http://dx.doi.org/10.3390/v14061215
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