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The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages

With the prospect of another pandemic Influenza fresh in our consciousness, the pathogenic nature of the Influenza A virus and its ability to induce high rates of mortality are ever more pertinent. Recently a novel protein encoded by an alternate reading frame in the PB1 Gene segment of Influenza A...

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Detalles Bibliográficos
Autor principal: Coleman, J Robert
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1781424/
https://www.ncbi.nlm.nih.gov/pubmed/17224071
http://dx.doi.org/10.1186/1743-422X-4-9
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author Coleman, J Robert
author_facet Coleman, J Robert
author_sort Coleman, J Robert
collection PubMed
description With the prospect of another pandemic Influenza fresh in our consciousness, the pathogenic nature of the Influenza A virus and its ability to induce high rates of mortality are ever more pertinent. Recently a novel protein encoded by an alternate reading frame in the PB1 Gene segment of Influenza A virus has been discovered and in turn shown to enhance viral virulence in a mouse model [1]. This protein has been shown to specifically target and destroy alveolar macrophages [2]. This review suggests that this protein, present in all previous pandemic strains, may reappear as a virulence factor in a subsequent pandemic strain. This PB1-F2 protein will enhance the mortality rate of the virus by increasing the likelihood of a secondary bacterial infection, which is the primary cause of death to a patient infected with Influenza A.
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spelling pubmed-17814242007-01-25 The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages Coleman, J Robert Virol J Commentary With the prospect of another pandemic Influenza fresh in our consciousness, the pathogenic nature of the Influenza A virus and its ability to induce high rates of mortality are ever more pertinent. Recently a novel protein encoded by an alternate reading frame in the PB1 Gene segment of Influenza A virus has been discovered and in turn shown to enhance viral virulence in a mouse model [1]. This protein has been shown to specifically target and destroy alveolar macrophages [2]. This review suggests that this protein, present in all previous pandemic strains, may reappear as a virulence factor in a subsequent pandemic strain. This PB1-F2 protein will enhance the mortality rate of the virus by increasing the likelihood of a secondary bacterial infection, which is the primary cause of death to a patient infected with Influenza A. BioMed Central 2007-01-15 /pmc/articles/PMC1781424/ /pubmed/17224071 http://dx.doi.org/10.1186/1743-422X-4-9 Text en Copyright © 2007 Coleman; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Commentary
Coleman, J Robert
The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages
title The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages
title_full The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages
title_fullStr The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages
title_full_unstemmed The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages
title_short The PB1-F2 protein of Influenza A virus: increasing pathogenicity by disrupting alveolar macrophages
title_sort pb1-f2 protein of influenza a virus: increasing pathogenicity by disrupting alveolar macrophages
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1781424/
https://www.ncbi.nlm.nih.gov/pubmed/17224071
http://dx.doi.org/10.1186/1743-422X-4-9
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