Evidence for a novel gene associated with human influenza A viruses
Identifieur interne : 000A59 ( Pmc/Checkpoint ); précédent : 000A58; suivant : 000A60Evidence for a novel gene associated with human influenza A viruses
Auteurs : Monica Clifford [Canada] ; James Twigg [Canada] ; Chris Upton [Canada]Source :
- Virology Journal [ 1743-422X ] ; 2009.
Abstract
Influenza A virus genomes are comprised of 8 negative strand single-stranded RNA segments and are thought to encode 11 proteins, which are all translated from mRNAs complementary to the genomic strands. Although human, swine and avian influenza A viruses are very similar, cross-species infections are usually limited. However, antigenic differences are considerable and when viruses become established in a different host or if novel viruses are created by re-assortment devastating pandemics may arise.
Examination of influenza A virus genomes from the early 20th Century revealed the association of a 167 codon ORF encoded by the genomic strand of segment 8 with human isolates. Close to the timing of the 1948
We hypothesize that the genomic strand of segment 8 of encodes a novel influenza A virus protein. The persistence and conservation of this genomic strand ORF for almost a century in human influenza A viruses provides strong evidence that it is translated into a polypeptide that enhances viral fitness in the human host. This has important consequences for the interpretation of experiments that utilize mutations in the NS1 and NEP genes of segment 8 and also for the consideration of events that may alter the spread and/or pathogenesis of swine and avian influenza A viruses in the human population.
Url:
DOI: 10.1186/1743-422X-6-198
PubMed: 19917120
PubMed Central: 2780412
Affiliations:
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PMC:2780412Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Evidence for a novel gene associated with human influenza A viruses</title>
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<author><name sortKey="Twigg, James" sort="Twigg, James" uniqKey="Twigg J" first="James" last="Twigg">James Twigg</name>
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<series><title level="j">Virology Journal</title>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Influenza A virus genomes are comprised of 8 negative strand single-stranded RNA segments and are thought to encode 11 proteins, which are all translated from mRNAs complementary to the genomic strands. Although human, swine and avian influenza A viruses are very similar, cross-species infections are usually limited. However, antigenic differences are considerable and when viruses become established in a different host or if novel viruses are created by re-assortment devastating pandemics may arise.</p>
</sec>
<sec><title>Results</title>
<p>Examination of influenza A virus genomes from the early 20<sup>th </sup>
Century revealed the association of a 167 codon ORF encoded by the genomic strand of segment 8 with human isolates. Close to the timing of the 1948 <italic>pseudopandemic</italic>
, a mutation occurred that resulted in the extension of this ORF to 216 codons. Since 1948, this ORF has been almost totally maintained in human influenza A viruses suggesting a selectable biological function. The discovery of cytotoxic T cells responding to an epitope encoded by this ORF suggests that it is translated into protein. Evidence of several other <italic>non-traditionally </italic>
translated polypeptides in influenza A virus support the translation of this genomic strand ORF. The gene product is predicted to have a signal sequence and two transmembrane domains.</p>
</sec>
<sec><title>Conclusion</title>
<p>We hypothesize that the genomic strand of segment 8 of encodes a novel influenza A virus protein. The persistence and conservation of this genomic strand ORF for almost a century in human influenza A viruses provides strong evidence that it is translated into a polypeptide that enhances viral fitness in the human host. This has important consequences for the interpretation of experiments that utilize mutations in the NS1 and NEP genes of segment 8 and also for the consideration of events that may alter the spread and/or pathogenesis of swine and avian influenza A viruses in the human population.</p>
</sec>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Virol J</journal-id>
<journal-title-group><journal-title>Virology Journal</journal-title>
</journal-title-group>
<issn pub-type="epub">1743-422X</issn>
<publisher><publisher-name>BioMed Central</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">19917120</article-id>
<article-id pub-id-type="pmc">2780412</article-id>
<article-id pub-id-type="publisher-id">1743-422X-6-198</article-id>
<article-id pub-id-type="doi">10.1186/1743-422X-6-198</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research</subject>
</subj-group>
</article-categories>
<title-group><article-title>Evidence for a novel gene associated with human influenza A viruses</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" id="A1"><name><surname>Clifford</surname>
<given-names>Monica</given-names>
</name>
<xref ref-type="aff" rid="I1">1</xref>
<email>mcliffor@uvic.ca</email>
</contrib>
<contrib contrib-type="author" id="A2"><name><surname>Twigg</surname>
<given-names>James</given-names>
</name>
<xref ref-type="aff" rid="I1">1</xref>
<email>jtwigg@uvic.ca</email>
</contrib>
<contrib contrib-type="author" corresp="yes" id="A3"><name><surname>Upton</surname>
<given-names>Chris</given-names>
</name>
<xref ref-type="aff" rid="I1">1</xref>
<email>cupton@uvic.ca</email>
</contrib>
</contrib-group>
<aff id="I1"><label>1</label>
Department of Biochemistry and Microbiology, University of Victoria, Victoria, BC, V8W 3P6, Canada</aff>
<pub-date pub-type="collection"><year>2009</year>
</pub-date>
<pub-date pub-type="epub"><day>16</day>
<month>11</month>
<year>2009</year>
</pub-date>
<volume>6</volume>
<fpage>198</fpage>
<lpage>198</lpage>
<history><date date-type="received"><day>15</day>
<month>10</month>
<year>2009</year>
</date>
<date date-type="accepted"><day>16</day>
<month>11</month>
<year>2009</year>
</date>
</history>
<permissions><copyright-statement>Copyright ©2009 Clifford et al; licensee BioMed Central Ltd.</copyright-statement>
<copyright-year>2009</copyright-year>
<copyright-holder>Clifford et al; licensee BioMed Central Ltd.</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/2.0"><license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/2.0">http://creativecommons.org/licenses/by/2.0</ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<self-uri xlink:href="http://www.virologyj.com/content/6/1/198"></self-uri>
<abstract><sec><title>Background</title>
<p>Influenza A virus genomes are comprised of 8 negative strand single-stranded RNA segments and are thought to encode 11 proteins, which are all translated from mRNAs complementary to the genomic strands. Although human, swine and avian influenza A viruses are very similar, cross-species infections are usually limited. However, antigenic differences are considerable and when viruses become established in a different host or if novel viruses are created by re-assortment devastating pandemics may arise.</p>
</sec>
<sec><title>Results</title>
<p>Examination of influenza A virus genomes from the early 20<sup>th </sup>
Century revealed the association of a 167 codon ORF encoded by the genomic strand of segment 8 with human isolates. Close to the timing of the 1948 <italic>pseudopandemic</italic>
, a mutation occurred that resulted in the extension of this ORF to 216 codons. Since 1948, this ORF has been almost totally maintained in human influenza A viruses suggesting a selectable biological function. The discovery of cytotoxic T cells responding to an epitope encoded by this ORF suggests that it is translated into protein. Evidence of several other <italic>non-traditionally </italic>
translated polypeptides in influenza A virus support the translation of this genomic strand ORF. The gene product is predicted to have a signal sequence and two transmembrane domains.</p>
</sec>
<sec><title>Conclusion</title>
<p>We hypothesize that the genomic strand of segment 8 of encodes a novel influenza A virus protein. The persistence and conservation of this genomic strand ORF for almost a century in human influenza A viruses provides strong evidence that it is translated into a polypeptide that enhances viral fitness in the human host. This has important consequences for the interpretation of experiments that utilize mutations in the NS1 and NEP genes of segment 8 and also for the consideration of events that may alter the spread and/or pathogenesis of swine and avian influenza A viruses in the human population.</p>
</sec>
</abstract>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Canada</li>
</country>
</list>
<tree><country name="Canada"><noRegion><name sortKey="Clifford, Monica" sort="Clifford, Monica" uniqKey="Clifford M" first="Monica" last="Clifford">Monica Clifford</name>
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<name sortKey="Twigg, James" sort="Twigg, James" uniqKey="Twigg J" first="James" last="Twigg">James Twigg</name>
<name sortKey="Upton, Chris" sort="Upton, Chris" uniqKey="Upton C" first="Chris" last="Upton">Chris Upton</name>
</country>
</tree>
</affiliations>
</record>
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