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Herpesviral Latency—Common Themes
Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167855/ https://www.ncbi.nlm.nih.gov/pubmed/32075270 http://dx.doi.org/10.3390/pathogens9020125 |
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author | Weidner-Glunde, Magdalena Kruminis-Kaszkiel, Ewa Savanagouder, Mamata |
author_facet | Weidner-Glunde, Magdalena Kruminis-Kaszkiel, Ewa Savanagouder, Mamata |
author_sort | Weidner-Glunde, Magdalena |
collection | PubMed |
description | Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency. |
format | Online Article Text |
id | pubmed-7167855 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-71678552020-04-21 Herpesviral Latency—Common Themes Weidner-Glunde, Magdalena Kruminis-Kaszkiel, Ewa Savanagouder, Mamata Pathogens Review Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency. MDPI 2020-02-15 /pmc/articles/PMC7167855/ /pubmed/32075270 http://dx.doi.org/10.3390/pathogens9020125 Text en © 2020 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Weidner-Glunde, Magdalena Kruminis-Kaszkiel, Ewa Savanagouder, Mamata Herpesviral Latency—Common Themes |
title | Herpesviral Latency—Common Themes |
title_full | Herpesviral Latency—Common Themes |
title_fullStr | Herpesviral Latency—Common Themes |
title_full_unstemmed | Herpesviral Latency—Common Themes |
title_short | Herpesviral Latency—Common Themes |
title_sort | herpesviral latency—common themes |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7167855/ https://www.ncbi.nlm.nih.gov/pubmed/32075270 http://dx.doi.org/10.3390/pathogens9020125 |
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