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Independence of Evolutionary and Mutational Rates after Transmission of Avian Influenza Viruses to Swine

Identifieur interne : 000147 ( Pmc/Curation ); précédent : 000146; suivant : 000148

Independence of Evolutionary and Mutational Rates after Transmission of Avian Influenza Viruses to Swine

Auteurs : J. Stech ; X. Xiong ; C. Scholtissek ; R. G. Webster

Source :

RBID : PMC:104428

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.


Url:
PubMed: 9971766
PubMed Central: 104428

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PMC:104428

Le document en format XML

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<p>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.</p>
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<journal-title>Journal of Virology</journal-title>
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<subject>Recombination and Evolution</subject>
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<article-title>Independence of Evolutionary and Mutational Rates after Transmission of Avian Influenza Viruses to Swine</article-title>
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<xref ref-type="author-notes" rid="FN150">*</xref>
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<aff id="N0x96dd4d8.0xa386af0"> Department of Virology and Molecular Biology
<sup>1</sup>
and Department of Epidemiology and Biostatistics,
<sup>2</sup>
St. Jude Children’s Research Hospital, Memphis, Tennessee 38105-2794</aff>
<author-notes>
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<label>*</label>
<p>Corresponding author. Mailing address: Department of Virology and Molecular Biology, St. Jude Children’s Research Hospital, 332 N. Lauderdale St., Memphis, TN 38105-2794. Phone: (901) 495-3400. Fax: (901) 495-2622. E-mail:
<email>Robert.Webster@stjude.org</email>
.</p>
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<p>Present address: Waldstrasse 53, Linden-Leihgestern 35440, Germany.</p>
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<pub-date pub-type="ppub">
<month>3</month>
<year>1999</year>
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<volume>73</volume>
<issue>3</issue>
<fpage>1878</fpage>
<lpage>1884</lpage>
<history>
<date date-type="received">
<day>9</day>
<month>3</month>
<year>1998</year>
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<date date-type="accepted">
<day>11</day>
<month>11</month>
<year>1998</year>
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<copyright-statement>Copyright © 1999, American Society for Microbiology</copyright-statement>
<copyright-year>1999</copyright-year>
<abstract>
<p>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.</p>
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