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Article: Molecular changes in the polymerase genes (PA and PB1) associated with high pathogenicity of H5N1 influenza virus in mallard ducks

TitleMolecular changes in the polymerase genes (PA and PB1) associated with high pathogenicity of H5N1 influenza virus in mallard ducks
Authors
Issue Date2007
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2007, v. 81 n. 16, p. 8515-8524 How to Cite?
AbstractThe highly pathogenic (HP) influenza viruses H5 and H7 are usually nonpathogenic in mallard ducks. However, the currently circulating HP H5N1 viruses acquired a different phenotype and are able to cause mortality in mallards. To establish the molecular basis of this phenotype, we cloned the human A/Vietnam/1203/04 (H5N1) influenza virus isolate that is highly pathogenic in ferrets, mice, and mallards and found it to be a heterogeneous mixture. Large-plaque isolates were highly pathogenic to ducks, mice, and ferrets, whereas small-plaque isolates were nonpathogenic in these species. Sequence analysis of the entire genome revealed that the small-plaque and the large-plaque isolates differed in the coding of five amino acids. There were two differences in the hemagglutinin (HA) gene (K52T and A544V), one in the PA gene (T515A), and two in the PB1 gene (K207R and Y436H). We inserted the amino acid changes into the wild-type reverse genetic virus construct to assess their effects on pathogenicity in vivo. The HA gene mutations and the PB1 gene K207R mutation did not alter the HP phenotype of the large-plaque virus, whereas constructs with the PA (T515A) and PB1 (Y436H) gene mutations were nonpathogenic in orally inoculated ducks. The PB1 (Y436H) construct was not efficiently transmitted in ducks, whereas the PA (T515A) construct replicated as well as the wild-type virus did and was transmitted efficiently. These results show that the PA and PB1 genes of HP H5N1 influenza viruses are associated with lethality in ducks. The mechanisms of lethality and the perpetuation of this lethal phenotype in ducks in nature remain to be determined. Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179802
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHulsePost, DJen_US
dc.contributor.authorFranks, Jen_US
dc.contributor.authorBoyd, Ken_US
dc.contributor.authorSalomon, Ren_US
dc.contributor.authorHoffmann, Een_US
dc.contributor.authorYen, HLen_US
dc.contributor.authorWebby, RJen_US
dc.contributor.authorWalker, Den_US
dc.contributor.authorNguyen, TDen_US
dc.contributor.authorWebster, RGen_US
dc.date.accessioned2012-12-19T10:04:56Z-
dc.date.available2012-12-19T10:04:56Z-
dc.date.issued2007en_US
dc.identifier.citationJournal Of Virology, 2007, v. 81 n. 16, p. 8515-8524en_US
dc.identifier.issn0022-538Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/179802-
dc.description.abstractThe highly pathogenic (HP) influenza viruses H5 and H7 are usually nonpathogenic in mallard ducks. However, the currently circulating HP H5N1 viruses acquired a different phenotype and are able to cause mortality in mallards. To establish the molecular basis of this phenotype, we cloned the human A/Vietnam/1203/04 (H5N1) influenza virus isolate that is highly pathogenic in ferrets, mice, and mallards and found it to be a heterogeneous mixture. Large-plaque isolates were highly pathogenic to ducks, mice, and ferrets, whereas small-plaque isolates were nonpathogenic in these species. Sequence analysis of the entire genome revealed that the small-plaque and the large-plaque isolates differed in the coding of five amino acids. There were two differences in the hemagglutinin (HA) gene (K52T and A544V), one in the PA gene (T515A), and two in the PB1 gene (K207R and Y436H). We inserted the amino acid changes into the wild-type reverse genetic virus construct to assess their effects on pathogenicity in vivo. The HA gene mutations and the PB1 gene K207R mutation did not alter the HP phenotype of the large-plaque virus, whereas constructs with the PA (T515A) and PB1 (Y436H) gene mutations were nonpathogenic in orally inoculated ducks. The PB1 (Y436H) construct was not efficiently transmitted in ducks, whereas the PA (T515A) construct replicated as well as the wild-type virus did and was transmitted efficiently. These results show that the PA and PB1 genes of HP H5N1 influenza viruses are associated with lethality in ducks. The mechanisms of lethality and the perpetuation of this lethal phenotype in ducks in nature remain to be determined. Copyright © 2007, American Society for Microbiology. All Rights Reserved.en_US
dc.languageengen_US
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_US
dc.relation.ispartofJournal of Virologyen_US
dc.subject.meshAmino Acid Substitutionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDna Mutational Analysisen_US
dc.subject.meshDucks - Virologyen_US
dc.subject.meshFerrets - Virologyen_US
dc.subject.meshGenome, Viral - Geneticsen_US
dc.subject.meshHemagglutinin Glycoproteins, Influenza Virus - Geneticsen_US
dc.subject.meshInfluenza A Virus, H5n1 Subtype - Genetics - Pathogenicityen_US
dc.subject.meshInfluenza In Birds - Virologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMutationen_US
dc.subject.meshRna Replicase - Geneticsen_US
dc.subject.meshViral Proteins - Geneticsen_US
dc.subject.meshVirulence - Geneticsen_US
dc.titleMolecular changes in the polymerase genes (PA and PB1) associated with high pathogenicity of H5N1 influenza virus in mallard ducksen_US
dc.typeArticleen_US
dc.identifier.emailYen, HL: hyen@hku.hken_US
dc.identifier.authorityYen, HL=rp00304en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1128/JVI.00435-07en_US
dc.identifier.pmid17553873-
dc.identifier.scopuseid_2-s2.0-34547779411en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34547779411&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume81en_US
dc.identifier.issue16en_US
dc.identifier.spage8515en_US
dc.identifier.epage8524en_US
dc.identifier.isiWOS:000248649100014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHulsePost, DJ=11940084300en_US
dc.identifier.scopusauthoridFranks, J=12786180500en_US
dc.identifier.scopusauthoridBoyd, K=7102417684en_US
dc.identifier.scopusauthoridSalomon, R=12786463900en_US
dc.identifier.scopusauthoridHoffmann, E=7201369718en_US
dc.identifier.scopusauthoridYen, HL=7102476668en_US
dc.identifier.scopusauthoridWebby, RJ=35448064800en_US
dc.identifier.scopusauthoridWalker, D=7404440465en_US
dc.identifier.scopusauthoridNguyen, TD=25227791100en_US
dc.identifier.scopusauthoridWebster, RG=36048363100en_US

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