Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus.
Identifieur interne : 000842 ( PubMed/Corpus ); précédent : 000841; suivant : 000843Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus.
Auteurs : Michael Worobey ; Guan-Zhu Han ; Andrew RambautSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2014.
English descriptors
- KwdEn :
- Adult, Aged, Animals, Biological Evolution, Birds, Child, Disease Resistance (immunology), Genetic Variation, Humans, Influenza A Virus, H1N1 Subtype (genetics), Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza A Virus, H3N2 Subtype (genetics), Influenza A Virus, H3N2 Subtype (immunology), Influenza A Virus, H3N2 Subtype (pathogenicity), Influenza A Virus, H3N8 Subtype (genetics), Influenza A Virus, H3N8 Subtype (immunology), Influenza A Virus, H3N8 Subtype (pathogenicity), Influenza A Virus, H5N1 Subtype (genetics), Influenza A Virus, H5N1 Subtype (immunology), Influenza A Virus, H5N1 Subtype (pathogenicity), Influenza A Virus, H7N9 Subtype (genetics), Influenza A Virus, H7N9 Subtype (immunology), Influenza A Virus, H7N9 Subtype (pathogenicity), Influenza A virus (genetics), Influenza A virus (immunology), Influenza A virus (pathogenicity), Influenza Pandemic, 1918-1919 (mortality), Influenza, Human (mortality), Influenza, Human (virology), Phylogeny, Reassortant Viruses (genetics), Reassortant Viruses (immunology), Reassortant Viruses (pathogenicity), Swine, Virulence.
- MESH :
- genetics : Influenza A Virus, H1N1 Subtype, Influenza A Virus, H3N2 Subtype, Influenza A Virus, H3N8 Subtype, Influenza A Virus, H5N1 Subtype, Influenza A Virus, H7N9 Subtype, Influenza A virus, Reassortant Viruses.
- immunology : Disease Resistance, Influenza A Virus, H1N1 Subtype, Influenza A Virus, H3N2 Subtype, Influenza A Virus, H3N8 Subtype, Influenza A Virus, H5N1 Subtype, Influenza A Virus, H7N9 Subtype, Influenza A virus, Reassortant Viruses.
- mortality : Influenza Pandemic, 1918-1919, Influenza, Human.
- pathogenicity : Influenza A Virus, H1N1 Subtype, Influenza A Virus, H3N2 Subtype, Influenza A Virus, H3N8 Subtype, Influenza A Virus, H5N1 Subtype, Influenza A Virus, H7N9 Subtype, Influenza A virus, Reassortant Viruses.
- virology : Influenza, Human.
- Adult, Aged, Animals, Biological Evolution, Birds, Child, Genetic Variation, Humans, Phylogeny, Swine, Virulence.
Abstract
The source, timing, and geographical origin of the 1918-1920 pandemic influenza A virus have remained tenaciously obscure for nearly a century, as have the reasons for its unusual severity among young adults. Here, we reconstruct the origins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineages using a host-specific molecular clock approach that is demonstrably more accurate than previous methods. Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before ∼1907, acquired avian N1 neuraminidase and internal protein genes. We find that the resulting pandemic virus jumped directly to swine but was likely displaced in humans by ∼1922 by a reassortant with an antigenically distinct H1 HA. Hence, although the swine lineage was a direct descendent of the pandemic virus, the post-1918 seasonal H1N1 lineage evidently was not, at least for HA. These findings help resolve several seemingly disparate observations from 20th century influenza epidemiology, seroarcheology, and immunology. The phylogenetic results, combined with these other lines of evidence, suggest that the high mortality in 1918 among adults aged ∼20 to ∼40 y may have been due primarily to their childhood exposure to a doubly heterosubtypic putative H3N8 virus, which we estimate circulated from ∼1889-1900. All other age groups (except immunologically naive infants) were likely partially protected by childhood exposure to N1 and/or H1-related antigens. Similar processes may underlie age-specific mortality differences between seasonal H1N1 vs. H3N2 and human H5N1 vs. H7N9 infections.
DOI: 10.1073/pnas.1324197111
PubMed: 24778238
Links to Exploration step
pubmed:24778238Le document en format XML
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Here, we reconstruct the origins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineages using a host-specific molecular clock approach that is demonstrably more accurate than previous methods. Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before ∼1907, acquired avian N1 neuraminidase and internal protein genes. We find that the resulting pandemic virus jumped directly to swine but was likely displaced in humans by ∼1922 by a reassortant with an antigenically distinct H1 HA. Hence, although the swine lineage was a direct descendent of the pandemic virus, the post-1918 seasonal H1N1 lineage evidently was not, at least for HA. These findings help resolve several seemingly disparate observations from 20th century influenza epidemiology, seroarcheology, and immunology. The phylogenetic results, combined with these other lines of evidence, suggest that the high mortality in 1918 among adults aged ∼20 to ∼40 y may have been due primarily to their childhood exposure to a doubly heterosubtypic putative H3N8 virus, which we estimate circulated from ∼1889-1900. All other age groups (except immunologically naive infants) were likely partially protected by childhood exposure to N1 and/or H1-related antigens. Similar processes may underlie age-specific mortality differences between seasonal H1N1 vs. H3N2 and human H5N1 vs. H7N9 infections. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24778238</PMID><DateCompleted><Year>2014</Year><Month>08</Month><Day>20</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>111</Volume><Issue>22</Issue><PubDate><Year>2014</Year><Month>Jun</Month><Day>03</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus.</ArticleTitle><Pagination><MedlinePgn>8107-12</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1324197111</ELocationID><Abstract><AbstractText>The source, timing, and geographical origin of the 1918-1920 pandemic influenza A virus have remained tenaciously obscure for nearly a century, as have the reasons for its unusual severity among young adults. Here, we reconstruct the origins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineages using a host-specific molecular clock approach that is demonstrably more accurate than previous methods. Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before ∼1907, acquired avian N1 neuraminidase and internal protein genes. We find that the resulting pandemic virus jumped directly to swine but was likely displaced in humans by ∼1922 by a reassortant with an antigenically distinct H1 HA. Hence, although the swine lineage was a direct descendent of the pandemic virus, the post-1918 seasonal H1N1 lineage evidently was not, at least for HA. These findings help resolve several seemingly disparate observations from 20th century influenza epidemiology, seroarcheology, and immunology. The phylogenetic results, combined with these other lines of evidence, suggest that the high mortality in 1918 among adults aged ∼20 to ∼40 y may have been due primarily to their childhood exposure to a doubly heterosubtypic putative H3N8 virus, which we estimate circulated from ∼1889-1900. All other age groups (except immunologically naive infants) were likely partially protected by childhood exposure to N1 and/or H1-related antigens. Similar processes may underlie age-specific mortality differences between seasonal H1N1 vs. H3N2 and human H5N1 vs. H7N9 infections. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Worobey</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721; worobey@email.arizona.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Guan-Zhu</ForeName><Initials>GZ</Initials><AffiliationInfo><Affiliation>Department of Ecology and Evolutionary Biology, University of Arizona, Tucson, AZ 85721;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rambaut</LastName><ForeName>Andrew</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute of Evolutionary Biology andCentre for Infection, Immunity, and Evolution, University of Edinburgh, Edinburgh EH9 3JT, United Kingdom; andFogarty International Center, National Institutes of Health, Bethesda, MD 20892.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>095831</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>260864</GrantID><Agency>European Research Council</Agency><Country>International</Country></Grant><Grant><GrantID>R01 AI084691</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>092807</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>04</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United 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