Risk assessment of H2N2 influenza viruses from the avian reservoir.
Identifieur interne : 000088 ( PubMed/Checkpoint ); précédent : 000087; suivant : 000089Risk assessment of H2N2 influenza viruses from the avian reservoir.
Auteurs : Jeremy C. Jones [États-Unis] ; Tatiana Baranovich ; Bindumadhav M. Marathe ; Angela F. Danner ; Jon P. Seiler ; John Franks ; Elena A. Govorkova ; Scott Krauss ; Robert G. WebsterSource :
- Journal of virology [ 1098-5514 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Animaux sauvages (virologie), Furets, Grippe chez les oiseaux (virologie), Grippe humaine (virologie), Humains, Lignée cellulaire, Oiseaux, Réplication virale, Réservoirs d'agents pathogènes (virologie), Souris, Souris de lignée DBA, Sous-type H2N2 du virus de la grippe A (génétique), Sous-type H2N2 du virus de la grippe A (isolement et purification), Sous-type H2N2 du virus de la grippe A (pathogénicité), Sous-type H2N2 du virus de la grippe A (physiologie), Suidae, Évaluation des risques.
- MESH :
- génétique : Sous-type H2N2 du virus de la grippe A.
- isolement et purification : Sous-type H2N2 du virus de la grippe A.
- pathogénicité : Sous-type H2N2 du virus de la grippe A.
- physiologie : Sous-type H2N2 du virus de la grippe A.
- virologie : Animaux sauvages, Grippe chez les oiseaux, Grippe humaine, Réservoirs d'agents pathogènes.
- Animaux, Furets, Humains, Lignée cellulaire, Oiseaux, Réplication virale, Souris, Souris de lignée DBA, Suidae, Évaluation des risques.
English descriptors
- KwdEn :
- Animals, Animals, Wild (virology), Birds, Cell Line, Disease Reservoirs (virology), Ferrets, Humans, Influenza A Virus, H2N2 Subtype (genetics), Influenza A Virus, H2N2 Subtype (isolation & purification), Influenza A Virus, H2N2 Subtype (pathogenicity), Influenza A Virus, H2N2 Subtype (physiology), Influenza in Birds (virology), Influenza, Human (virology), Mice, Mice, Inbred DBA, Risk Assessment, Swine, Virus Replication.
- MESH :
- genetics : Influenza A Virus, H2N2 Subtype.
- isolation & purification : Influenza A Virus, H2N2 Subtype.
- pathogenicity : Influenza A Virus, H2N2 Subtype.
- physiology : Influenza A Virus, H2N2 Subtype.
- virology : Animals, Wild, Disease Reservoirs, Influenza in Birds, Influenza, Human.
- Animals, Birds, Cell Line, Ferrets, Humans, Mice, Mice, Inbred DBA, Risk Assessment, Swine, Virus Replication.
Abstract
H2N2 influenza A viruses were the cause of the 1957-1958 pandemic. Historical evidence demonstrates they arose from avian virus ancestors, and while the H2N2 subtype has disappeared from humans, it persists in wild and domestic birds. Reemergence of H2N2 in humans is a significant threat due to the absence of humoral immunity in individuals under the age of 50. Thus, examination of these viruses, particularly those from the avian reservoir, must be addressed through surveillance, characterization, and antiviral testing. The data presented here are a risk assessment of 22 avian H2N2 viruses isolated from wild and domestic birds over 6 decades. Our data show that they have a low rate of genetic and antigenic evolution and remained similar to isolates circulating near the time of the pandemic. Most isolates replicated in mice and human bronchial epithelial cells, but replication in swine tissues was low or absent. Multiple isolates replicated in ferrets, and 3 viruses were transmitted to direct-contact cage mates. Markers of mammalian adaptation in hemagglutinin (HA) and PB2 proteins were absent from all isolates, and they retained a preference for avian-like α2,3-linked sialic acid receptors. Most isolates remained antigenically similar to pandemic A/Singapore/1/57 (H2N2) virus, suggesting they could be controlled by the pandemic vaccine candidate. All viruses were susceptible to neuraminidase inhibitors and adamantanes. Nonetheless, the sustained pathogenicity of avian H2N2 viruses in multiple mammalian models elevates their risk potential for human infections and stresses the need for continual surveillance as a component of prepandemic planning.
DOI: 10.1128/JVI.02526-13
PubMed: 24227848
Affiliations:
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Historical evidence demonstrates they arose from avian virus ancestors, and while the H2N2 subtype has disappeared from humans, it persists in wild and domestic birds. Reemergence of H2N2 in humans is a significant threat due to the absence of humoral immunity in individuals under the age of 50. Thus, examination of these viruses, particularly those from the avian reservoir, must be addressed through surveillance, characterization, and antiviral testing. The data presented here are a risk assessment of 22 avian H2N2 viruses isolated from wild and domestic birds over 6 decades. Our data show that they have a low rate of genetic and antigenic evolution and remained similar to isolates circulating near the time of the pandemic. Most isolates replicated in mice and human bronchial epithelial cells, but replication in swine tissues was low or absent. Multiple isolates replicated in ferrets, and 3 viruses were transmitted to direct-contact cage mates. Markers of mammalian adaptation in hemagglutinin (HA) and PB2 proteins were absent from all isolates, and they retained a preference for avian-like α2,3-linked sialic acid receptors. Most isolates remained antigenically similar to pandemic A/Singapore/1/57 (H2N2) virus, suggesting they could be controlled by the pandemic vaccine candidate. All viruses were susceptible to neuraminidase inhibitors and adamantanes. Nonetheless, the sustained pathogenicity of avian H2N2 viruses in multiple mammalian models elevates their risk potential for human infections and stresses the need for continual surveillance as a component of prepandemic planning. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24227848</PMID><DateCompleted><Year>2014</Year><Month>03</Month><Day>10</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>88</Volume><Issue>2</Issue><PubDate><Year>2014</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Risk assessment of H2N2 influenza viruses from the avian reservoir.</ArticleTitle><Pagination><MedlinePgn>1175-88</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.02526-13</ELocationID><Abstract><AbstractText>H2N2 influenza A viruses were the cause of the 1957-1958 pandemic. Historical evidence demonstrates they arose from avian virus ancestors, and while the H2N2 subtype has disappeared from humans, it persists in wild and domestic birds. Reemergence of H2N2 in humans is a significant threat due to the absence of humoral immunity in individuals under the age of 50. Thus, examination of these viruses, particularly those from the avian reservoir, must be addressed through surveillance, characterization, and antiviral testing. The data presented here are a risk assessment of 22 avian H2N2 viruses isolated from wild and domestic birds over 6 decades. Our data show that they have a low rate of genetic and antigenic evolution and remained similar to isolates circulating near the time of the pandemic. Most isolates replicated in mice and human bronchial epithelial cells, but replication in swine tissues was low or absent. Multiple isolates replicated in ferrets, and 3 viruses were transmitted to direct-contact cage mates. Markers of mammalian adaptation in hemagglutinin (HA) and PB2 proteins were absent from all isolates, and they retained a preference for avian-like α2,3-linked sialic acid receptors. Most isolates remained antigenically similar to pandemic A/Singapore/1/57 (H2N2) virus, suggesting they could be controlled by the pandemic vaccine candidate. All viruses were susceptible to neuraminidase inhibitors and adamantanes. Nonetheless, the sustained pathogenicity of avian H2N2 viruses in multiple mammalian models elevates their risk potential for human infections and stresses the need for continual surveillance as a component of prepandemic planning. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>Jeremy C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baranovich</LastName><ForeName>Tatiana</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Marathe</LastName><ForeName>Bindumadhav M</ForeName><Initials>BM</Initials></Author><Author ValidYN="Y"><LastName>Danner</LastName><ForeName>Angela F</ForeName><Initials>AF</Initials></Author><Author ValidYN="Y"><LastName>Seiler</LastName><ForeName>Jon P</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Franks</LastName><ForeName>John</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Govorkova</LastName><ForeName>Elena A</ForeName><Initials>EA</Initials></Author><Author ValidYN="Y"><LastName>Krauss</LastName><ForeName>Scott</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Webster</LastName><ForeName>Robert G</ForeName><Initials>RG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HHSN272200900007C</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01AI30071</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HHSN272200900007C</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01-AI30071</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><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>2013</Year><Month>11</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000835" MajorTopicYN="N">Animals, Wild</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001717" MajorTopicYN="N">Birds</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004197" MajorTopicYN="N">Disease Reservoirs</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005289" MajorTopicYN="N">Ferrets</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="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005585" MajorTopicYN="N">Influenza in Birds</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008811" MajorTopicYN="N">Mice, Inbred DBA</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013552" MajorTopicYN="N">Swine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate 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Danner</name><name sortKey="Franks, John" sort="Franks, John" uniqKey="Franks J" first="John" last="Franks">John Franks</name><name sortKey="Govorkova, Elena A" sort="Govorkova, Elena A" uniqKey="Govorkova E" first="Elena A" last="Govorkova">Elena A. Govorkova</name><name sortKey="Krauss, Scott" sort="Krauss, Scott" uniqKey="Krauss S" first="Scott" last="Krauss">Scott Krauss</name><name sortKey="Marathe, Bindumadhav M" sort="Marathe, Bindumadhav M" uniqKey="Marathe B" first="Bindumadhav M" last="Marathe">Bindumadhav M. Marathe</name><name sortKey="Seiler, Jon P" sort="Seiler, Jon P" uniqKey="Seiler J" first="Jon P" last="Seiler">Jon P. Seiler</name><name sortKey="Webster, Robert G" sort="Webster, Robert G" uniqKey="Webster R" first="Robert G" last="Webster">Robert G. Webster</name></noCountry><country name="États-Unis"><region name="Tennessee"><name sortKey="Jones, Jeremy C" sort="Jones, Jeremy C" uniqKey="Jones J" first="Jeremy C" last="Jones">Jeremy C. 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