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Article: Inefficient transmission of H5N1 influenza viruses in a ferret contact model

TitleInefficient transmission of H5N1 influenza viruses in a ferret contact model
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. 13, p. 6890-6898 How to Cite?
AbstractThe abilities to infect and transmit efficiently among humans are essential for a novel influenza A virus to cause a pandemic. To evaluate the pandemic potential of widely disseminated H5N1 influenza viruses, a ferret contact model using experimental groups comprised of one inoculated ferret and two contact ferrets was used to study the transmissibility of four human H5N1 viruses isolated from 2003 to 2006. The effects of viral pathogenicity and receptor binding specificity (affinity to synthetic sialosaccharides with α2,3 or α2,6 linkages) on transmissibility were assessed. A/Vietnam/1203/04 and A/Vietnam/JP36-2/05 viruses, which possess "avian-like" α2,3-linked sialic acid (SA) receptor specificity, caused neurological symptoms and death in ferrets inoculated with 103 50% tissue culture infectious doses. A/Hong Kong/213/03 and A/Turkey/65-596/06 viruses, which show binding affinity for "human-like" α2,6-linked SA receptors in addition to their affinity for α2,3-linked SA receptors, caused mild clinical symptoms and were not lethal to the ferrets. No transmission of A/Vietnam/1203/04 or A/Turkey/65-596/06 virus was detected. One contact ferret developed neutralizing antibodies to A/Hong Kong/213/03 but did not exhibit any clinical signs or detectable virus shedding. In two groups, one of two naïve contact ferrets had detectable virus after 6 to 8 days when housed together with the A/Vietnam/JP36-2/05 virus-inoculated ferrets. Infected contact ferrets showed severe clinical signs, although little or no virus was detected in nasal washes. This limited virus shedding explained the absence of secondary transmission from the infected contact ferret to the other naive ferret that were housed together. Our results suggest that despite their receptor binding affinity, circulating H5N1 viruses retain molecular determinants that restrict their spread among mammalian species. Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179801
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYen, HLen_US
dc.contributor.authorLipatov, ASen_US
dc.contributor.authorIlyushina, NAen_US
dc.contributor.authorGovorkova, EAen_US
dc.contributor.authorFranks, Jen_US
dc.contributor.authorYilmaz, Nen_US
dc.contributor.authorDouglas, Aen_US
dc.contributor.authorHay, Aen_US
dc.contributor.authorKrauss, Sen_US
dc.contributor.authorRehg, JEen_US
dc.contributor.authorHoffmann, Een_US
dc.contributor.authorWebster, RGen_US
dc.date.accessioned2012-12-19T10:04:55Z-
dc.date.available2012-12-19T10:04:55Z-
dc.date.issued2007en_US
dc.identifier.citationJournal Of Virology, 2007, v. 81 n. 13, p. 6890-6898en_US
dc.identifier.issn0022-538Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/179801-
dc.description.abstractThe abilities to infect and transmit efficiently among humans are essential for a novel influenza A virus to cause a pandemic. To evaluate the pandemic potential of widely disseminated H5N1 influenza viruses, a ferret contact model using experimental groups comprised of one inoculated ferret and two contact ferrets was used to study the transmissibility of four human H5N1 viruses isolated from 2003 to 2006. The effects of viral pathogenicity and receptor binding specificity (affinity to synthetic sialosaccharides with α2,3 or α2,6 linkages) on transmissibility were assessed. A/Vietnam/1203/04 and A/Vietnam/JP36-2/05 viruses, which possess "avian-like" α2,3-linked sialic acid (SA) receptor specificity, caused neurological symptoms and death in ferrets inoculated with 103 50% tissue culture infectious doses. A/Hong Kong/213/03 and A/Turkey/65-596/06 viruses, which show binding affinity for "human-like" α2,6-linked SA receptors in addition to their affinity for α2,3-linked SA receptors, caused mild clinical symptoms and were not lethal to the ferrets. No transmission of A/Vietnam/1203/04 or A/Turkey/65-596/06 virus was detected. One contact ferret developed neutralizing antibodies to A/Hong Kong/213/03 but did not exhibit any clinical signs or detectable virus shedding. In two groups, one of two naïve contact ferrets had detectable virus after 6 to 8 days when housed together with the A/Vietnam/JP36-2/05 virus-inoculated ferrets. Infected contact ferrets showed severe clinical signs, although little or no virus was detected in nasal washes. This limited virus shedding explained the absence of secondary transmission from the infected contact ferret to the other naive ferret that were housed together. Our results suggest that despite their receptor binding affinity, circulating H5N1 viruses retain molecular determinants that restrict their spread among mammalian species. 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.meshAnimalsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDisease Outbreaksen_US
dc.subject.meshFerrets - Immunology - Virologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInfluenza A Virus, H5n1 Subtype - Immunology - Pathogenicityen_US
dc.subject.meshNasal Cavity - Pathology - Virologyen_US
dc.subject.meshOrthomyxoviridae Infections - Epidemiology - Immunology - Pathology - Transmissionen_US
dc.subject.meshSpecies Specificityen_US
dc.subject.meshVirus Shedding - Immunologyen_US
dc.titleInefficient transmission of H5N1 influenza viruses in a ferret contact modelen_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.00170-07en_US
dc.identifier.pmid17459930-
dc.identifier.scopuseid_2-s2.0-34250829563en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34250829563&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume81en_US
dc.identifier.issue13en_US
dc.identifier.spage6890en_US
dc.identifier.epage6898en_US
dc.identifier.isiWOS:000247404900012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYen, HL=7102476668en_US
dc.identifier.scopusauthoridLipatov, AS=7005117347en_US
dc.identifier.scopusauthoridIlyushina, NA=6506741015en_US
dc.identifier.scopusauthoridGovorkova, EA=7003837718en_US
dc.identifier.scopusauthoridFranks, J=12786180500en_US
dc.identifier.scopusauthoridYilmaz, N=16647702000en_US
dc.identifier.scopusauthoridDouglas, A=7202732750en_US
dc.identifier.scopusauthoridHay, A=7201696824en_US
dc.identifier.scopusauthoridKrauss, S=7102769210en_US
dc.identifier.scopusauthoridRehg, JE=7004835777en_US
dc.identifier.scopusauthoridHoffmann, E=7201369718en_US
dc.identifier.scopusauthoridWebster, RG=36048363100en_US
dc.identifier.issnl0022-538X-

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