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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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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2007
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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. |
format | Text |
id | pubmed-1781424 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
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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