Recombinant influenza virus with a pandemic H2N2 polymerase complex has a higher adaptive potential than one with seasonal H2N2 polymerase complex.
Identifieur interne : 000043 ( PubMed/Checkpoint ); précédent : 000042; suivant : 000044Recombinant influenza virus with a pandemic H2N2 polymerase complex has a higher adaptive potential than one with seasonal H2N2 polymerase complex.
Auteurs : Alex W H. Chin [République populaire de Chine] ; Hui-L Yen [République populaire de Chine] ; Scott Krauss [États-Unis] ; Richard J. Webby [États-Unis] ; Leo L M. Poon [République populaire de Chine]Source :
- The Journal of general virology [ 1465-2099 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Grippe humaine (virologie), Grippe humaine (épidémiologie), Humains, Mutation, Pandémies, Protéines virales (génétique), Protéines virales (métabolisme), RNA replicase (génétique), RNA replicase (métabolisme), Recombinaison génétique, Saisons, Sous-type H2N2 du virus de la grippe A (enzymologie), Sous-type H2N2 du virus de la grippe A (génétique), Sous-type H3N2 du virus de la grippe A (enzymologie), Sous-type H3N2 du virus de la grippe A (génétique), Virus recombinants (enzymologie), Virus recombinants (génétique), États-Unis d'Amérique (épidémiologie).
- MESH :
- enzymologie : Sous-type H2N2 du virus de la grippe A, Sous-type H3N2 du virus de la grippe A, Virus recombinants.
- génétique : Protéines virales, RNA replicase, Sous-type H2N2 du virus de la grippe A, Sous-type H3N2 du virus de la grippe A, Virus recombinants.
- métabolisme : Protéines virales, RNA replicase.
- virologie : Grippe humaine.
- épidémiologie : Grippe humaine, États-Unis d'Amérique.
- Animaux, Humains, Mutation, Pandémies, Recombinaison génétique, Saisons.
- Wicri :
- geographic : États-Unis.
English descriptors
- KwdEn :
- Animals, Humans, Influenza A Virus, H2N2 Subtype (enzymology), Influenza A Virus, H2N2 Subtype (genetics), Influenza A Virus, H3N2 Subtype (enzymology), Influenza A Virus, H3N2 Subtype (genetics), Influenza, Human (epidemiology), Influenza, Human (virology), Mutation, Pandemics, RNA Replicase (genetics), RNA Replicase (metabolism), Reassortant Viruses (enzymology), Reassortant Viruses (genetics), Recombination, Genetic, Seasons, United States (epidemiology), Viral Proteins (genetics), Viral Proteins (metabolism).
- MESH :
- chemical , genetics : RNA Replicase, Viral Proteins.
- geographic , epidemiology : United States.
- enzymology : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H3N2 Subtype, Reassortant Viruses.
- epidemiology : Influenza, Human.
- genetics : Influenza A Virus, H2N2 Subtype, Influenza A Virus, H3N2 Subtype, Reassortant Viruses.
- chemical , metabolism : RNA Replicase, Viral Proteins.
- virology : Influenza, Human.
- Animals, Humans, Mutation, Pandemics, Recombination, Genetic, Seasons.
Abstract
The reassortment of influenza viral gene segments plays a key role in the genesis of pandemic strains. All of the last three pandemic viruses contained reassorted polymerase complexes with subunits derived from animal viruses, suggesting that the acquisition of a reassorted polymerase complex might have a role in generating these pandemic viruses. Here, we studied polymerase activities of the pandemic H2N2, seasonal H2N2 and pandemic H3N2 viruses. We observed that the viral ribonucleoprotein (vRNP) of pandemic H2N2 virus has a highly robust activity. The polymerase activity of seasonal H2N2 viruses, however, was much reduced. We further identified three mutations (PB2-I114V, PB1-S261N and PA-D383N) responsible for the reduced activity. To determine the potential impact of viral polymerase activity on the viral life cycle, recombinant H3N2 viruses carrying pandemic and seasonal H2N2 vRNP were studied in cell cultures supplemented with oseltamivir carboxylate and tested for their abilities to develop adaptive or resistant mutations. It was found that the recombinant virus with pandemic H2N2 vRNP was more capable of restoring the viral fitness than the one with seasonal vRNP. These results suggest that a robust vRNP is advantageous to influenza virus to cope with a new selection pressure.
DOI: 10.1099/jgv.0.000385
PubMed: 26703222
Affiliations:
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All of the last three pandemic viruses contained reassorted polymerase complexes with subunits derived from animal viruses, suggesting that the acquisition of a reassorted polymerase complex might have a role in generating these pandemic viruses. Here, we studied polymerase activities of the pandemic H2N2, seasonal H2N2 and pandemic H3N2 viruses. We observed that the viral ribonucleoprotein (vRNP) of pandemic H2N2 virus has a highly robust activity. The polymerase activity of seasonal H2N2 viruses, however, was much reduced. We further identified three mutations (PB2-I114V, PB1-S261N and PA-D383N) responsible for the reduced activity. To determine the potential impact of viral polymerase activity on the viral life cycle, recombinant H3N2 viruses carrying pandemic and seasonal H2N2 vRNP were studied in cell cultures supplemented with oseltamivir carboxylate and tested for their abilities to develop adaptive or resistant mutations. It was found that the recombinant virus with pandemic H2N2 vRNP was more capable of restoring the viral fitness than the one with seasonal vRNP. These results suggest that a robust vRNP is advantageous to influenza virus to cope with a new selection pressure. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26703222</PMID><DateCompleted><Year>2016</Year><Month>07</Month><Day>25</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1465-2099</ISSN><JournalIssue CitedMedium="Internet"><Volume>97</Volume><Issue>3</Issue><PubDate><Year>2016</Year><Month>Mar</Month></PubDate></JournalIssue><Title>The Journal of general virology</Title><ISOAbbreviation>J. Gen. Virol.</ISOAbbreviation></Journal><ArticleTitle>Recombinant influenza virus with a pandemic H2N2 polymerase complex has a higher adaptive potential than one with seasonal H2N2 polymerase complex.</ArticleTitle><Pagination><MedlinePgn>611-619</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1099/jgv.0.000385</ELocationID><Abstract><AbstractText>The reassortment of influenza viral gene segments plays a key role in the genesis of pandemic strains. All of the last three pandemic viruses contained reassorted polymerase complexes with subunits derived from animal viruses, suggesting that the acquisition of a reassorted polymerase complex might have a role in generating these pandemic viruses. Here, we studied polymerase activities of the pandemic H2N2, seasonal H2N2 and pandemic H3N2 viruses. We observed that the viral ribonucleoprotein (vRNP) of pandemic H2N2 virus has a highly robust activity. The polymerase activity of seasonal H2N2 viruses, however, was much reduced. We further identified three mutations (PB2-I114V, PB1-S261N and PA-D383N) responsible for the reduced activity. To determine the potential impact of viral polymerase activity on the viral life cycle, recombinant H3N2 viruses carrying pandemic and seasonal H2N2 vRNP were studied in cell cultures supplemented with oseltamivir carboxylate and tested for their abilities to develop adaptive or resistant mutations. It was found that the recombinant virus with pandemic H2N2 vRNP was more capable of restoring the viral fitness than the one with seasonal vRNP. These results suggest that a robust vRNP is advantageous to influenza virus to cope with a new selection pressure. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chin</LastName><ForeName>Alex W H</ForeName><Initials>AWH</Initials><AffiliationInfo><Affiliation>Centre of Influenza Research & School of Public Health, University of Hong Kong, Hong Kong, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yen</LastName><ForeName>Hui-L</ForeName><Initials>HL</Initials><AffiliationInfo><Affiliation>Centre of Influenza Research & School of Public Health, University of Hong Kong, Hong Kong, PR China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krauss</LastName><ForeName>Scott</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Virology Division, Department of Infectious Diseases, St Jude Children's Research Hospital, Memphis, TN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Webby</LastName><ForeName>Richard J</ForeName><Initials>RJ</Initials><AffiliationInfo><Affiliation>Virology Division, Department of Infectious Diseases, St Jude Children's Research Hospital, Memphis, TN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Poon</LastName><ForeName>Leo L M</ForeName><Initials>LLM</Initials><AffiliationInfo><Affiliation>Centre of Influenza Research & School of Public Health, University of Hong Kong, Hong Kong, PR China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HSN266200700005C</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>12</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Gen Virol</MedlineTA><NlmUniqueID>0077340</NlmUniqueID><ISSNLinking>0022-1317</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C057027">PB2 protein, Influenzavirus A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.7.48</RegistryNumber><NameOfSubstance UI="D012324">RNA Replicase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053121" MajorTopicYN="N">Influenza A Virus, H2N2 Subtype</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053122" MajorTopicYN="N">Influenza A Virus, H3N2 Subtype</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012324" MajorTopicYN="N">RNA Replicase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016865" MajorTopicYN="N">Reassortant Viruses</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011995" MajorTopicYN="Y">Recombination, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012621" MajorTopicYN="N">Seasons</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014481" MajorTopicYN="N" Type="Geographic">United States</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014764" 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Chin</name></noRegion><name sortKey="Poon, Leo L M" sort="Poon, Leo L M" uniqKey="Poon L" first="Leo L M" last="Poon">Leo L M. Poon</name><name sortKey="Yen, Hui L" sort="Yen, Hui L" uniqKey="Yen H" first="Hui-L" last="Yen">Hui-L Yen</name></country><country name="États-Unis"><noRegion><name sortKey="Krauss, Scott" sort="Krauss, Scott" uniqKey="Krauss S" first="Scott" last="Krauss">Scott Krauss</name></noRegion><name sortKey="Webby, Richard J" sort="Webby, Richard J" uniqKey="Webby R" first="Richard J" last="Webby">Richard J. Webby</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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