Document Detail


PB1-F2 modulates early host responses but does not affect the pathogenesis of H1N1 seasonal influenza virus.
MedLine Citation:
PMID:  22318139     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the context of infections with highly pathogenic influenza A viruses, the PB1-F2 protein contributes to virulence and enhances lung inflammation. In contrast, its role in the pathogenesis of seasonal influenza viral strains is less clear, especially in the H1N1 subtype, where strains can have a full-length 87- to 90-amino-acid protein, a truncated 57-amino-acid version, or lack the protein altogether. Toward this, we introduced the full-length 1918 PB1-F2, or prevented PB1-F2 expression, in H1N1 A/USSR/90/77, a seasonal strain that naturally expresses a truncated PB1-F2. All viruses replicated with similar efficiency in ferret or macaque ex vivo lung cultures and elicited similar cytokine mRNA profiles. In contrast, the virus expressing the 1918 PB1-F2 protein caused a delay of proinflammatory responses in ferret blood-derived macrophages, while the PB1-F2 knockout virus resulted in a more rapid response. A similar but less pronounced delay in innate immune activation was also observed in the nasal wash cells of ferrets infected with the 1918 PB1-F2-expressing virus. However, the three viruses did not differ in their virulence or clinical course in ferrets, supporting speculations that PB1-F2 is of limited importance for the pathogenesis of primary viral infection with human seasonal H1N1 viruses.
Authors:
Isabelle Meunier; Veronika von Messling
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-02-08
Journal Detail:
Title:  Journal of virology     Volume:  86     ISSN:  1098-5514     ISO Abbreviation:  J. Virol.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-03-29     Completed Date:  2012-06-18     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0113724     Medline TA:  J Virol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4271-8     Citation Subset:  IM    
Affiliation:
INRS-Institut Armand-Frappier, University of Quebec, Laval, Quebec, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Cytokines / metabolism
Dogs
Ferrets
Humans
Influenza A Virus, H1N1 Subtype / genetics,  immunology*,  pathogenicity*
Interferon-alpha / metabolism
Interleukin-1beta / metabolism
Interleukin-6 / metabolism
Lung / metabolism,  pathology,  virology
Macaca fascicularis
Macrophages / immunology,  metabolism
Mutation
Viral Proteins / genetics,  metabolism*
Virulence / genetics
Virulence Factors / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
NIP-79937//Canadian Institutes of Health Research; PAN-310641//Canadian Institutes of Health Research; PAN-83146//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Cytokines; 0/Interferon-alpha; 0/Interleukin-1beta; 0/Interleukin-6; 0/PB1-F2 protein, Influenza A virus; 0/Viral Proteins; 0/Virulence Factors
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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