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Pleiotropic mechanisms of virus survival and persistence

Viruses are enormously efficient infectious agents that have been implicated in causing human disease for centuries. Transmission of these pathogens continues to be from one life form to another in the form of isolated cases, epidemics, and pandemics. Each infection requires entry into a susceptible...

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Detalles Bibliográficos
Autor principal: Miller, Craig S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Mosby, Inc. 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7118778/
https://www.ncbi.nlm.nih.gov/pubmed/16037790
http://dx.doi.org/10.1016/j.tripleo.2005.03.017
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author Miller, Craig S.
author_facet Miller, Craig S.
author_sort Miller, Craig S.
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description Viruses are enormously efficient infectious agents that have been implicated in causing human disease for centuries. Transmission of these pathogens continues to be from one life form to another in the form of isolated cases, epidemics, and pandemics. Each infection requires entry into a susceptible host, replication, and evasion of the immune system. Viruses are successful pathogens because they target specific cells for their attack, exploit the cellular machinery, and are efficient in circumventing and/or inhibiting key cellular events required of survival. This article reviews some of the advances that have taken place in human virology in the past 50 years, emphasizing mechanisms that contribute to, and are involved with, virus survival and persistence.
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spelling pubmed-71187782020-04-03 Pleiotropic mechanisms of virus survival and persistence Miller, Craig S. Oral Surg Oral Med Oral Pathol Oral Radiol Endod Article Viruses are enormously efficient infectious agents that have been implicated in causing human disease for centuries. Transmission of these pathogens continues to be from one life form to another in the form of isolated cases, epidemics, and pandemics. Each infection requires entry into a susceptible host, replication, and evasion of the immune system. Viruses are successful pathogens because they target specific cells for their attack, exploit the cellular machinery, and are efficient in circumventing and/or inhibiting key cellular events required of survival. This article reviews some of the advances that have taken place in human virology in the past 50 years, emphasizing mechanisms that contribute to, and are involved with, virus survival and persistence. Mosby, Inc. 2005-08 2005-07-16 /pmc/articles/PMC7118778/ /pubmed/16037790 http://dx.doi.org/10.1016/j.tripleo.2005.03.017 Text en Copyright © 2005 Mosby, Inc. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Miller, Craig S.
Pleiotropic mechanisms of virus survival and persistence
title Pleiotropic mechanisms of virus survival and persistence
title_full Pleiotropic mechanisms of virus survival and persistence
title_fullStr Pleiotropic mechanisms of virus survival and persistence
title_full_unstemmed Pleiotropic mechanisms of virus survival and persistence
title_short Pleiotropic mechanisms of virus survival and persistence
title_sort pleiotropic mechanisms of virus survival and persistence
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7118778/
https://www.ncbi.nlm.nih.gov/pubmed/16037790
http://dx.doi.org/10.1016/j.tripleo.2005.03.017
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