Independence of evolutionary and mutational rates after transmission of avian influenza viruses to swine.
Identifieur interne : 000377 ( PubMed/Curation ); précédent : 000376; suivant : 000378Independence of evolutionary and mutational rates after transmission of avian influenza viruses to swine.
Auteurs : J. Stech [États-Unis] ; X. Xiong ; C. Scholtissek ; R G WebsterSource :
- Journal of virology [ 0022-538X ] ; 1999.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Virus de la grippe A.
- virologie : Suidae.
- Animaux, Chiens, Infections à Orthomyxoviridae, Mutation, Réplication virale, Virus de la grippe A, Évolution biologique.
English descriptors
- KwdEn :
- MESH :
- classification : Influenza A virus.
- genetics : Influenza A virus.
- transmission : Orthomyxoviridae Infections.
- virology : Swine.
- Animals, Biological Evolution, Dogs, Mutation, Virus Replication.
Abstract
In 1979, an H1N1 avian influenza virus crossed the species barrier, establishing a new lineage in European swine. Because there is no direct or serologic evidence of previous H1N1 strains in these pigs, these isolates provide a model for studying early evolution of influenza viruses. The evolutionary rates of both the coding and noncoding changes of the H1N1 swine strains are higher than those of human and classic swine influenza A viruses. In addition, early H1N1 swine isolates show a marked plaque heterogeneity that consistently appears after a few passages. The presence of a mutator mutation was postulated (C. Scholtissek, S. Ludwig, and W. M. Fitch, Arch. Virol. 131:237-250, 1993) to account for these observations and the successful establishment of an avian H1N1 strain in swine. To address this question, we calculated the mutation rates of A/Mallard/New York/6750/78 (H2N2) and A/Swine/Germany/2/81 (H1N1) by using the frequency of amantadine-resistant mutants. To account for the inherent variability of estimated mutation rates, we used a probabilistic model for the statistical analysis. The resulting estimated mutation rates of the two strains were not significantly different. Therefore, an increased mutation rate due to the presence of a mutator mutation is unlikely to have led to the successful introduction of avian H1N1 viruses in European swine.
PubMed: 9971766
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Scholtissek</name></author><author><name sortKey="Webster, R G" sort="Webster, R G" uniqKey="Webster R" first="R G" last="Webster">R G Webster</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1999">1999</date><idno type="RBID">pubmed:9971766</idno><idno type="pmid">9971766</idno><idno type="wicri:Area/PubMed/Corpus">000377</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000377</idno><idno type="wicri:Area/PubMed/Curation">000377</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000377</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Independence of evolutionary and mutational rates after transmission of avian influenza viruses to swine.</title><author><name sortKey="Stech, J" sort="Stech, J" uniqKey="Stech J" first="J" last="Stech">J. Stech</name><affiliation wicri:level="1"><nlm:affiliation>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794</wicri:regionArea></affiliation></author><author><name sortKey="Xiong, X" sort="Xiong, X" uniqKey="Xiong X" first="X" last="Xiong">X. Xiong</name></author><author><name sortKey="Scholtissek, C" sort="Scholtissek, C" uniqKey="Scholtissek C" first="C" last="Scholtissek">C. Scholtissek</name></author><author><name sortKey="Webster, R G" sort="Webster, R G" uniqKey="Webster R" first="R G" last="Webster">R G Webster</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biological Evolution</term><term>Dogs</term><term>Influenza A virus (classification)</term><term>Influenza A virus (genetics)</term><term>Mutation</term><term>Orthomyxoviridae Infections (transmission)</term><term>Swine (virology)</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Chiens</term><term>Infections à Orthomyxoviridae (transmission)</term><term>Mutation</term><term>Réplication virale</term><term>Suidae (virologie)</term><term>Virus de la grippe A ()</term><term>Virus de la grippe A (génétique)</term><term>Évolution biologique</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="transmission" xml:lang="en"><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Suidae</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Swine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biological Evolution</term><term>Dogs</term><term>Mutation</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Chiens</term><term>Infections à Orthomyxoviridae</term><term>Mutation</term><term>Réplication virale</term><term>Virus de la grippe A</term><term>Évolution biologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In 1979, an H1N1 avian influenza virus crossed the species barrier, establishing a new lineage in European swine. Because there is no direct or serologic evidence of previous H1N1 strains in these pigs, these isolates provide a model for studying early evolution of influenza viruses. The evolutionary rates of both the coding and noncoding changes of the H1N1 swine strains are higher than those of human and classic swine influenza A viruses. In addition, early H1N1 swine isolates show a marked plaque heterogeneity that consistently appears after a few passages. The presence of a mutator mutation was postulated (C. Scholtissek, S. Ludwig, and W. M. Fitch, Arch. Virol. 131:237-250, 1993) to account for these observations and the successful establishment of an avian H1N1 strain in swine. To address this question, we calculated the mutation rates of A/Mallard/New York/6750/78 (H2N2) and A/Swine/Germany/2/81 (H1N1) by using the frequency of amantadine-resistant mutants. To account for the inherent variability of estimated mutation rates, we used a probabilistic model for the statistical analysis. The resulting estimated mutation rates of the two strains were not significantly different. Therefore, an increased mutation rate due to the presence of a mutator mutation is unlikely to have led to the successful introduction of avian H1N1 viruses in European swine.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9971766</PMID><DateCompleted><Year>1999</Year><Month>03</Month><Day>04</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>73</Volume><Issue>3</Issue><PubDate><Year>1999</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Independence of evolutionary and mutational rates after transmission of avian influenza viruses to swine.</ArticleTitle><Pagination><MedlinePgn>1878-84</MedlinePgn></Pagination><Abstract><AbstractText>In 1979, an H1N1 avian influenza virus crossed the species barrier, establishing a new lineage in European swine. Because there is no direct or serologic evidence of previous H1N1 strains in these pigs, these isolates provide a model for studying early evolution of influenza viruses. The evolutionary rates of both the coding and noncoding changes of the H1N1 swine strains are higher than those of human and classic swine influenza A viruses. In addition, early H1N1 swine isolates show a marked plaque heterogeneity that consistently appears after a few passages. The presence of a mutator mutation was postulated (C. Scholtissek, S. Ludwig, and W. M. Fitch, Arch. Virol. 131:237-250, 1993) to account for these observations and the successful establishment of an avian H1N1 strain in swine. To address this question, we calculated the mutation rates of A/Mallard/New York/6750/78 (H2N2) and A/Swine/Germany/2/81 (H1N1) by using the frequency of amantadine-resistant mutants. To account for the inherent variability of estimated mutation rates, we used a probabilistic model for the statistical analysis. The resulting estimated mutation rates of the two strains were not significantly different. 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IdType="pubmed">1600756</ArticleId></ArticleIdList></Reference><Reference><Citation>Genetics. 1943 Nov;28(6):491-511</Citation><ArticleIdList><ArticleId IdType="pubmed">17247100</ArticleId></ArticleIdList></Reference><Reference><Citation>Virology. 1991 Nov;185(1):291-8</Citation><ArticleIdList><ArticleId IdType="pubmed">1833874</ArticleId></ArticleIdList></Reference><Reference><Citation>J Gen Virol. 1976 Oct;33(1):143-5</Citation><ArticleIdList><ArticleId IdType="pubmed">185324</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 1991 Oct;65(10):5491-8</Citation><ArticleIdList><ArticleId IdType="pubmed">1895397</ArticleId></ArticleIdList></Reference><Reference><Citation>Virology. 1991 Jul;183(1):61-73</Citation><ArticleIdList><ArticleId IdType="pubmed">2053297</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 1990 Dec;64(12):6278-81</Citation><ArticleIdList><ArticleId IdType="pubmed">2173792</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Biol Evol. 1990 Mar;7(2):194-200</Citation><ArticleIdList><ArticleId IdType="pubmed">2319943</ArticleId></ArticleIdList></Reference><Reference><Citation>J Infect Dis. 1989 Jun;159(6):1050-6</Citation><ArticleIdList><ArticleId IdType="pubmed">2723453</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 1986 Aug;59(2):377-83</Citation><ArticleIdList><ArticleId IdType="pubmed">3016304</ArticleId></ArticleIdList></Reference><Reference><Citation>EMBO J. 1985 Nov;4(11):3021-4</Citation><ArticleIdList><ArticleId IdType="pubmed">4065098</ArticleId></ArticleIdList></Reference><Reference><Citation>Naturwissenschaften. 1977 Nov;64(11):541-65</Citation><ArticleIdList><ArticleId IdType="pubmed">593400</ArticleId></ArticleIdList></Reference><Reference><Citation>Bull World Health Organ. 1981;59(1):75-8</Citation><ArticleIdList><ArticleId IdType="pubmed">6973418</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1982 Mar 19;215(4539):1468-74</Citation><ArticleIdList><ArticleId IdType="pubmed">7038875</ArticleId></ArticleIdList></Reference><Reference><Citation>Virology. 1978 Sep;89(2):506-16</Citation><ArticleIdList><ArticleId IdType="pubmed">716216</ArticleId></ArticleIdList></Reference><Reference><Citation>Virology. 1995 Oct 1;212(2):555-61</Citation><ArticleIdList><ArticleId IdType="pubmed">7571425</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1995 Jan 27;267(5197):483-9</Citation><ArticleIdList><ArticleId IdType="pubmed">7824947</ArticleId></ArticleIdList></Reference><Reference><Citation>J Gen Virol. 1994 Feb;75 ( Pt 2):389-93</Citation><ArticleIdList><ArticleId IdType="pubmed">8113760</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 1994 May;68(5):3120-8</Citation><ArticleIdList><ArticleId IdType="pubmed">8151777</ArticleId></ArticleIdList></Reference><Reference><Citation>Arch Virol. 1993;131(3-4):237-50</Citation><ArticleIdList><ArticleId IdType="pubmed">8347076</ArticleId></ArticleIdList></Reference><Reference><Citation>FASEB J. 1996 Jun;10(8):859-64</Citation><ArticleIdList><ArticleId IdType="pubmed">8666162</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1997 Mar 21;275(5307):1793-6</Citation><ArticleIdList><ArticleId IdType="pubmed">9065404</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1997 Jun 12;387(6634):700-2</Citation><ArticleIdList><ArticleId IdType="pubmed">9192893</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):7712-8</Citation><ArticleIdList><ArticleId IdType="pubmed">9223253</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1997 Oct 9;389(6651):554</Citation><ArticleIdList><ArticleId IdType="pubmed">9335492</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1998 Jan 16;279(5349):393-6</Citation><ArticleIdList><ArticleId IdType="pubmed">9430591</ArticleId></ArticleIdList></Reference><Reference><Citation>AIDS. 1998 Mar 26;12(5):461-5</Citation><ArticleIdList><ArticleId IdType="pubmed">9543443</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1976 Sep 23;263(5575):285-9</Citation><ArticleIdList><ArticleId IdType="pubmed">958482</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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