Viral and Host Factors Required for Avian H5N1 Influenza A Virus Replication in Mammalian Cells
Identifieur interne : 000E33 ( Pmc/Curation ); précédent : 000E32; suivant : 000E34Viral and Host Factors Required for Avian H5N1 Influenza A Virus Replication in Mammalian Cells
Auteurs : Hong Zhang ; Benjamin G. Hale ; Ke Xu ; Bing Sun [République populaire de Chine]Source :
- Viruses [ 1999-4915 ] ; 2013.
Abstract
Following the initial and sporadic emergence into humans of highly pathogenic avian H5N1 influenza A viruses in Hong Kong in 1997, we have come to realize the potential for avian influenza A viruses to be transmitted directly from birds to humans. Understanding the basic viral and cellular mechanisms that contribute to infection of mammalian species with avian influenza viruses is essential for developing prevention and control measures against possible future human pandemics. Multiple physical and functional cellular barriers can restrict influenza A virus infection in a new host species, including the cell membrane, the nuclear envelope, the nuclear environment, and innate antiviral responses. In this review, we summarize current knowledge on viral and host factors required for avian H5N1 influenza A viruses to successfully establish infections in mammalian cells. We focus on the molecular mechanisms underpinning mammalian host restrictions, as well as the adaptive mutations that are necessary for an avian influenza virus to overcome them. It is likely that many more viral and host determinants remain to be discovered, and future research in this area should provide novel and translational insights into the biology of influenza virus-host interactions.
Url:
DOI: 10.3390/v5061431
PubMed: 23752648
PubMed Central: 3717715
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<front><div type="abstract" xml:lang="en"><p>Following the initial and sporadic emergence into humans of highly pathogenic avian H5N1 influenza A viruses in Hong Kong in 1997, we have come to realize the potential for avian influenza A viruses to be transmitted directly from birds to humans. Understanding the basic viral and cellular mechanisms that contribute to infection of mammalian species with avian influenza viruses is essential for developing prevention and control measures against possible future human pandemics. Multiple physical and functional cellular barriers can restrict influenza A virus infection in a new host species, including the cell membrane, the nuclear envelope, the nuclear environment, and innate antiviral responses. In this review, we summarize current knowledge on viral and host factors required for avian H5N1 influenza A viruses to successfully establish infections in mammalian cells. We focus on the molecular mechanisms underpinning mammalian host restrictions, as well as the adaptive mutations that are necessary for an avian influenza virus to overcome them. It is likely that many more viral and host determinants remain to be discovered, and future research in this area should provide novel and translational insights into the biology of influenza virus-host interactions.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Viruses</journal-id>
<journal-id journal-id-type="iso-abbrev">Viruses</journal-id>
<journal-id journal-id-type="publisher-id">viruses</journal-id>
<journal-title-group><journal-title>Viruses</journal-title>
</journal-title-group>
<issn pub-type="epub">1999-4915</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23752648</article-id>
<article-id pub-id-type="pmc">3717715</article-id>
<article-id pub-id-type="doi">10.3390/v5061431</article-id>
<article-id pub-id-type="publisher-id">viruses-05-01431</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Viral and Host Factors Required for Avian H5N1 Influenza A Virus Replication in Mammalian Cells</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Hong</given-names>
</name>
<xref ref-type="aff" rid="af1-viruses-05-01431">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Hale</surname>
<given-names>Benjamin G.</given-names>
</name>
<xref ref-type="aff" rid="af2-viruses-05-01431">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Xu</surname>
<given-names>Ke</given-names>
</name>
<xref ref-type="aff" rid="af1-viruses-05-01431">1</xref>
<xref rid="c1-viruses-05-01431" ref-type="corresp">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sun</surname>
<given-names>Bing</given-names>
</name>
<xref ref-type="aff" rid="af1-viruses-05-01431">1</xref>
<xref ref-type="aff" rid="af3-viruses-05-01431">3</xref>
<xref rid="c1-viruses-05-01431" ref-type="corresp">*</xref>
</contrib>
</contrib-group>
<aff id="af1-viruses-05-01431"><label>1</label>
Molecular Virus Unit, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Shanghai institutes for Biological Sciences, Chinese Academy of Sciences, 225 South Chongqing Road, Shanghai 200025, China; E-Mail:<email>zhanghong@sibs.ac.cn</email>
</aff>
<aff id="af2-viruses-05-01431"><label>2</label>
Medical Research Council (MRC), University of Glasgow Centre for Virus Research, 8 Church Street, Glasgow, G11 5JR, Scotland, UK; E-Mail:<email>ben.hale@glasgow.ac.uk</email>
</aff>
<aff id="af3-viruses-05-01431"><label>3</label>
Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China</aff>
<author-notes><corresp id="c1-viruses-05-01431"><label>*</label>
Authors to whom correspondence should be addressed; E-Mails: <email>kxu@sibs.ac.cn</email>
(K.X.); <email>bsun@sibs.ac.cn</email>
(B.S.); Tel.: +86-21-6385-1929 (K.X.); +86-21-6385-1927 (B.S.); Fax: +86-21-6384-3571 (K.X. and B.S.).</corresp>
</author-notes>
<pub-date pub-type="epub"><day>10</day>
<month>6</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="collection"><month>6</month>
<year>2013</year>
</pub-date>
<volume>5</volume>
<issue>6</issue>
<fpage>1431</fpage>
<lpage>1446</lpage>
<history><date date-type="received"><day>05</day>
<month>12</month>
<year>2012</year>
</date>
<date date-type="rev-recd"><day>07</day>
<month>2</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>23</day>
<month>5</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>© 2013 by the authors; licensee MDPI, Basel, Switzerland.</copyright-statement>
<copyright-year>2013</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/3.0/"><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/3.0/">http://creativecommons.org/licenses/by/3.0/</ext-link>
).</license-p>
</license>
</permissions>
<abstract><p>Following the initial and sporadic emergence into humans of highly pathogenic avian H5N1 influenza A viruses in Hong Kong in 1997, we have come to realize the potential for avian influenza A viruses to be transmitted directly from birds to humans. Understanding the basic viral and cellular mechanisms that contribute to infection of mammalian species with avian influenza viruses is essential for developing prevention and control measures against possible future human pandemics. Multiple physical and functional cellular barriers can restrict influenza A virus infection in a new host species, including the cell membrane, the nuclear envelope, the nuclear environment, and innate antiviral responses. In this review, we summarize current knowledge on viral and host factors required for avian H5N1 influenza A viruses to successfully establish infections in mammalian cells. We focus on the molecular mechanisms underpinning mammalian host restrictions, as well as the adaptive mutations that are necessary for an avian influenza virus to overcome them. It is likely that many more viral and host determinants remain to be discovered, and future research in this area should provide novel and translational insights into the biology of influenza virus-host interactions.</p>
</abstract>
<kwd-group><kwd>avian H5N1influenza A viruses</kwd>
<kwd>replication in mammalian cells</kwd>
<kwd>molecular mechanisms</kwd>
<kwd>adaptive mutation</kwd>
<kwd>species barrier</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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