Comparison of Avian and Human Influenza A Viruses Reveals a Mutational Bias on the Viral Genomes▿
Identifieur interne : 000382 ( Pmc/Corpus ); précédent : 000381; suivant : 000383Comparison of Avian and Human Influenza A Viruses Reveals a Mutational Bias on the Viral Genomes▿
Auteurs : Raul Rabadan ; Arnold J. Levine ; Harlan RobinsSource :
- Journal of Virology [ 0022-538X ] ; 2006.
Abstract
In the last few years, the genomic sequence data for thousands of influenza A virus strains, including the 1918 pandemic strain, and hundreds of isolates of the avian influenza virus H5N1, which is causing an increasing number of human fatalities, have become publicly available. This large quantity of sequence data allows us to do comparative genomics with the human and avian versions of the virus. We find that the nucleotide compositions of influenza A viruses infecting the two hosts are sufficiently different that we can determine the host at almost 100% accuracy. This assignment works at the segment level, which allows us to construct the reassortment history of individual segments within each strain. We suggest that the different nucleotide compositions can be explained by a host-dependent mutation bias. To support this idea, we estimate the fixation rates for the different polymerase segments and the ratios of synonymous to nonsynonymous changes. Additionally, we provide evidence supporting the hypothesis that the H1N1 influenza virus entered the human population just prior to the 1918 outbreak, with an earliest bound of 1910.
Url:
DOI: 10.1128/JVI.01414-06
PubMed: 16987977
PubMed Central: 1642607
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PMC:1642607Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>In the last few years, the genomic sequence data for thousands of influenza A virus strains, including the 1918 pandemic strain, and hundreds of isolates of the avian influenza virus H5N1, which is causing an increasing number of human fatalities, have become publicly available. This large quantity of sequence data allows us to do comparative genomics with the human and avian versions of the virus. We find that the nucleotide compositions of influenza A viruses infecting the two hosts are sufficiently different that we can determine the host at almost 100% accuracy. This assignment works at the segment level, which allows us to construct the reassortment history of individual segments within each strain. We suggest that the different nucleotide compositions can be explained by a host-dependent mutation bias. To support this idea, we estimate the fixation rates for the different polymerase segments and the ratios of synonymous to nonsynonymous changes. Additionally, we provide evidence supporting the hypothesis that the H1N1 influenza virus entered the human population just prior to the 1918 outbreak, with an earliest bound of 1910.</p>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Virol</journal-id>
<journal-id journal-id-type="publisher-id">jvi</journal-id>
<journal-title>Journal of Virology</journal-title>
<issn pub-type="ppub">0022-538X</issn>
<issn pub-type="epub">1098-5514</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
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<article-id pub-id-type="pmc">1642607</article-id>
<article-id pub-id-type="publisher-id">1414-06</article-id>
<article-id pub-id-type="doi">10.1128/JVI.01414-06</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Genetic Diversity and Evolution</subject>
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<title-group><article-title>Comparison of Avian and Human Influenza A Viruses Reveals a Mutational Bias on the Viral Genomes<xref ref-type="fn" rid="fn1">▿</xref>
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<contrib-group><contrib contrib-type="author"><name><surname>Rabadan</surname>
<given-names>Raul</given-names>
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<xref ref-type="aff" rid="aff1">1</xref>
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<contrib contrib-type="author"><name><surname>Levine</surname>
<given-names>Arnold J.</given-names>
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<xref ref-type="aff" rid="aff1">1</xref>
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<contrib contrib-type="author"><name><surname>Robins</surname>
<given-names>Harlan</given-names>
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<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff1">2</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
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<aff id="aff1">Institute for Advanced Study, Einstein Dr., Princeton, New Jersey 08540,<label>1</label>
Computational Biology Group, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N, Seattle, Washington 98109<label>2</label>
</aff>
<author-notes><fn id="cor1"><label>*</label>
<p>Corresponding author. Mailing address: Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Mail Stop M2-B876, Seattle, WA 98105. Phone: (206) 667-2571. Fax: (206) 667-1319. E-mail: <email>hrobins@fhcrc.org</email>
.</p>
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<pub-date pub-type="ppub"><month>12</month>
<year>2006</year>
</pub-date>
<pub-date pub-type="epub"><day>20</day>
<month>9</month>
<year>2006</year>
</pub-date>
<volume>80</volume>
<issue>23</issue>
<fpage>11887</fpage>
<lpage>11891</lpage>
<history><date date-type="received"><day>5</day>
<month>7</month>
<year>2006</year>
</date>
<date date-type="accepted"><day>11</day>
<month>9</month>
<year>2006</year>
</date>
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<copyright-statement>Copyright © 2006, American Society for Microbiology</copyright-statement>
<copyright-year>2006</copyright-year>
<self-uri xlink:title="pdf" xlink:href="zjv02306011887.pdf"></self-uri>
<abstract><p>In the last few years, the genomic sequence data for thousands of influenza A virus strains, including the 1918 pandemic strain, and hundreds of isolates of the avian influenza virus H5N1, which is causing an increasing number of human fatalities, have become publicly available. This large quantity of sequence data allows us to do comparative genomics with the human and avian versions of the virus. We find that the nucleotide compositions of influenza A viruses infecting the two hosts are sufficiently different that we can determine the host at almost 100% accuracy. This assignment works at the segment level, which allows us to construct the reassortment history of individual segments within each strain. We suggest that the different nucleotide compositions can be explained by a host-dependent mutation bias. To support this idea, we estimate the fixation rates for the different polymerase segments and the ratios of synonymous to nonsynonymous changes. Additionally, we provide evidence supporting the hypothesis that the H1N1 influenza virus entered the human population just prior to the 1918 outbreak, with an earliest bound of 1910.</p>
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