Investigation of Influenza Virus Polymerase Activity in Pig Cells
Identifieur interne : 000604 ( Pmc/Checkpoint ); précédent : 000603; suivant : 000605Investigation of Influenza Virus Polymerase Activity in Pig Cells
Auteurs : Olivier Moncorgé [Royaume-Uni] ; Jason S. Long [Royaume-Uni] ; Anna V. Cauldwell [Royaume-Uni] ; Hongbo Zhou [Royaume-Uni] ; Samantha J. Lycett [Royaume-Uni] ; Wendy S. Barclay [Royaume-Uni]Source :
- Journal of Virology [ 0022-538X ] ; 2013.
Abstract
Reassortant influenza viruses with combinations of avian, human, and/or swine genomic segments have been detected frequently in pigs. As a consequence, pigs have been accused of being a “mixing vessel” for influenza viruses. This implies that pig cells support transcription and replication of avian influenza viruses, in contrast to human cells, in which most avian influenza virus polymerases display limited activity. Although influenza virus polymerase activity has been studied in human and avian cells for many years by use of a minigenome assay, similar investigations in pig cells have not been reported. We developed the first minigenome assay for pig cells and compared the activities of polymerases of avian or human influenza virus origin in pig, human, and avian cells. We also investigated in pig cells the consequences of some known mammalian host range determinants that enhance influenza virus polymerase activity in human cells, such as PB2 mutations E627K, D701N, G590S/Q591R, and T271A. The two typical avian influenza virus polymerases used in this study were poorly active in pig cells, similar to what is seen in human cells, and mutations that adapt the avian influenza virus polymerase for human cells also increased activity in pig cells. In contrast, a different pattern was observed in avian cells. Finally, highly pathogenic avian influenza virus H5N1 polymerase activity was tested because this subtype has been reported to replicate only poorly in pigs. H5N1 polymerase was active in swine cells, suggesting that other barriers restrict these viruses from becoming endemic in pigs.
Url:
DOI: 10.1128/JVI.01633-12
PubMed: 23077313
PubMed Central: 3536367
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Reassortant influenza viruses with combinations of avian, human, and/or swine genomic segments have been detected frequently in pigs. As a consequence, pigs have been accused of being a “mixing vessel” for influenza viruses. This implies that pig cells support transcription and replication of avian influenza viruses, in contrast to human cells, in which most avian influenza virus polymerases display limited activity. Although influenza virus polymerase activity has been studied in human and avian cells for many years by use of a minigenome assay, similar investigations in pig cells have not been reported. We developed the first minigenome assay for pig cells and compared the activities of polymerases of avian or human influenza virus origin in pig, human, and avian cells. We also investigated in pig cells the consequences of some known mammalian host range determinants that enhance influenza virus polymerase activity in human cells, such as PB2 mutations E627K, D701N, G590S/Q591R, and T271A. The two typical avian influenza virus polymerases used in this study were poorly active in pig cells, similar to what is seen in human cells, and mutations that adapt the avian influenza virus polymerase for human cells also increased activity in pig cells. In contrast, a different pattern was observed in avian cells. Finally, highly pathogenic avian influenza virus H5N1 polymerase activity was tested because this subtype has been reported to replicate only poorly in pigs. H5N1 polymerase was active in swine cells, suggesting that other barriers restrict these viruses from becoming endemic in pigs.</p>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Virol</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Virol</journal-id>
<journal-id journal-id-type="hwp">jvi</journal-id>
<journal-id journal-id-type="pmc">jvi</journal-id>
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<article-id pub-id-type="publisher-id">01633-12</article-id>
<article-id pub-id-type="doi">10.1128/JVI.01633-12</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Genome Replication and Regulation of Viral Gene Expression</subject>
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<title-group><article-title>Investigation of Influenza Virus Polymerase Activity in Pig Cells</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Moncorgé</surname>
<given-names>Olivier</given-names>
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<xref ref-type="aff" rid="aff1"><sup>a</sup>
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<xref ref-type="aff" rid="aff1"><sup>a</sup>
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<contrib contrib-type="author"><name><surname>Cauldwell</surname>
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<xref ref-type="aff" rid="aff1"><sup>a</sup>
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<contrib contrib-type="author"><name><surname>Zhou</surname>
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<xref ref-type="aff" rid="aff1"><sup>a</sup>
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<given-names>Samantha J.</given-names>
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<xref ref-type="aff" rid="aff2"><sup>b</sup>
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<contrib contrib-type="author" corresp="yes"><name><surname>Barclay</surname>
<given-names>Wendy S.</given-names>
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Section of Virology, Department of Medicine, Imperial College London, St. Mary's Campus, London, United Kingdom</aff>
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Institute of Evolutionary Biology, University of Edinburgh, Ashworth Laboratories, Edinburgh, United Kingdom</aff>
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<author-notes><corresp>Address correspondence to Wendy S. Barclay, <email>w.barclay@imperial.ac.uk</email>
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<pub-date pub-type="ppub"><month>1</month>
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<volume>87</volume>
<issue>1</issue>
<fpage>384</fpage>
<lpage>394</lpage>
<history><date date-type="received"><day>28</day>
<month>6</month>
<year>2012</year>
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<date date-type="accepted"><day>12</day>
<month>10</month>
<year>2012</year>
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<permissions><copyright-statement>Copyright © 2013, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2013</copyright-year>
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<abstract><p>Reassortant influenza viruses with combinations of avian, human, and/or swine genomic segments have been detected frequently in pigs. As a consequence, pigs have been accused of being a “mixing vessel” for influenza viruses. This implies that pig cells support transcription and replication of avian influenza viruses, in contrast to human cells, in which most avian influenza virus polymerases display limited activity. Although influenza virus polymerase activity has been studied in human and avian cells for many years by use of a minigenome assay, similar investigations in pig cells have not been reported. We developed the first minigenome assay for pig cells and compared the activities of polymerases of avian or human influenza virus origin in pig, human, and avian cells. We also investigated in pig cells the consequences of some known mammalian host range determinants that enhance influenza virus polymerase activity in human cells, such as PB2 mutations E627K, D701N, G590S/Q591R, and T271A. The two typical avian influenza virus polymerases used in this study were poorly active in pig cells, similar to what is seen in human cells, and mutations that adapt the avian influenza virus polymerase for human cells also increased activity in pig cells. In contrast, a different pattern was observed in avian cells. Finally, highly pathogenic avian influenza virus H5N1 polymerase activity was tested because this subtype has been reported to replicate only poorly in pigs. H5N1 polymerase was active in swine cells, suggesting that other barriers restrict these viruses from becoming endemic in pigs.</p>
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