Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus.
Identifieur interne : 000E55 ( Main/Curation ); précédent : 000E54; suivant : 000E56Genesis and pathogenesis of the 1918 pandemic H1N1 influenza A virus.
Auteurs : Michael Worobey [États-Unis] ; Guan-Zhu Han [États-Unis] ; Andrew Rambaut [États-Unis]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2014.
Descripteurs français
- KwdFr :
- Adulte, Animaux, Enfant, Grippe humaine (mortalité), Grippe humaine (virologie), Humains, Oiseaux, Pandémie de grippe de 1918-1919 (mortalité), Phylogénie, Résistance à la maladie (immunologie), Sous-type H1N1 du virus de la grippe A (génétique), Sous-type H1N1 du virus de la grippe A (immunologie), Sous-type H1N1 du virus de la grippe A (pathogénicité), Sous-type H3N2 du virus de la grippe A (génétique), Sous-type H3N2 du virus de la grippe A (immunologie), Sous-type H3N2 du virus de la grippe A (pathogénicité), Sous-type H3N8 du virus de la grippe A (génétique), Sous-type H3N8 du virus de la grippe A (immunologie), Sous-type H3N8 du virus de la grippe A (pathogénicité), Sous-type H5N1 du virus de la grippe A (génétique), Sous-type H5N1 du virus de la grippe A (immunologie), Sous-type H5N1 du virus de la grippe A (pathogénicité), Sous-type H7N9 du virus de la grippe A (génétique), Sous-type H7N9 du virus de la grippe A (immunologie), Sous-type H7N9 du virus de la grippe A (pathogénicité), Suidae, Sujet âgé, Variation génétique, Virulence, Virus de la grippe A (génétique), Virus de la grippe A (immunologie), Virus de la grippe A (pathogénicité), Virus recombinants (génétique), Virus recombinants (immunologie), Virus recombinants (pathogénicité), Évolution biologique.
- MESH :
- génétique : Sous-type H1N1 du virus de la grippe A, Sous-type H3N2 du virus de la grippe A, Sous-type H3N8 du virus de la grippe A, Sous-type H5N1 du virus de la grippe A, Sous-type H7N9 du virus de la grippe A, Virus de la grippe A, Virus recombinants.
- immunologie : Résistance à la maladie, Sous-type H1N1 du virus de la grippe A, Sous-type H3N2 du virus de la grippe A, Sous-type H3N8 du virus de la grippe A, Sous-type H5N1 du virus de la grippe A, Sous-type H7N9 du virus de la grippe A, Virus de la grippe A, Virus recombinants.
- mortalité : Grippe humaine, Pandémie de grippe de 1918-1919.
- pathogénicité : Sous-type H1N1 du virus de la grippe A, Sous-type H3N2 du virus de la grippe A, Sous-type H3N8 du virus de la grippe A, Sous-type H5N1 du virus de la grippe A, Sous-type H7N9 du virus de la grippe A, Virus de la grippe A, Virus recombinants.
- virologie : Grippe humaine.
- Adulte, Animaux, Enfant, Humains, Oiseaux, Phylogénie, Suidae, Sujet âgé, Variation génétique, Virulence, Évolution biologique.
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
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xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term><term>Sous-type H3N2 du virus de la grippe A</term><term>Sous-type H3N8 du virus de la grippe A</term><term>Sous-type H5N1 du virus de la grippe A</term><term>Sous-type H7N9 du virus de la grippe A</term><term>Virus de la grippe A</term><term>Virus recombinants</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Animals</term><term>Biological Evolution</term><term>Birds</term><term>Child</term><term>Genetic Variation</term><term>Humans</term><term>Phylogeny</term><term>Swine</term><term>Virulence</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Animaux</term><term>Enfant</term><term>Humains</term><term>Oiseaux</term><term>Phylogénie</term><term>Suidae</term><term>Sujet âgé</term><term>Variation génétique</term><term>Virulence</term><term>Évolution biologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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. </div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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