Influenza A Virus Entry: Implications in Virulence and Future Therapeutics
Identifieur interne : 000876 ( Main/Exploration ); précédent : 000875; suivant : 000877Influenza A Virus Entry: Implications in Virulence and Future Therapeutics
Auteurs : Emily Rumschlag-Booms [États-Unis] ; Lijun Rong [États-Unis]Source :
- Advances in Virology [ 1687-8639 ] ; 2013.
Abstract
Influenza A viruses have broad host tropism, being able to infect a range of hosts from wild fowl to swine to humans. This broad tropism makes highly pathogenic influenza A strains, such as H5N1, potentially dangerous to humans if they gain the ability to jump from an animal reservoir to humans. How influenza A viruses are able to jump the species barrier is incompletely understood due to the complex genetic nature of the viral surface glycoprotein, hemagglutinin, which mediates entry, combined with the virus's ability to use various receptor linkages. Current therapeutics against influenza A include those that target the uncoating process after entry as well as those that prevent viral budding. While there are therapeutics in development that target entry, currently there are none clinically available. We review here the genetics of influenza A viruses that contribute to entry tropism, how these genetic alterations may contribute to receptor usage and species tropism, as well as how novel therapeutics can be developed that target the major surface glycoprotein, hemagglutinin.
Url:
DOI: 10.1155/2013/121924
PubMed: 23365574
PubMed Central: 3556402
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Influenza A viruses have broad host tropism, being able to infect a range of hosts from wild fowl to swine to humans. This broad tropism makes highly pathogenic influenza A strains, such as H5N1, potentially dangerous to humans if they gain the ability to jump from an animal reservoir to humans. How influenza A viruses are able to jump the species barrier is incompletely understood due to the complex genetic nature of the viral surface glycoprotein, hemagglutinin, which mediates entry, combined with the virus's ability to use various receptor linkages. Current therapeutics against influenza A include those that target the uncoating process after entry as well as those that prevent viral budding. While there are therapeutics in development that target entry, currently there are none clinically available. We review here the genetics of influenza A viruses that contribute to entry tropism, how these genetic alterations may contribute to receptor usage and species tropism, as well as how novel therapeutics can be developed that target the major surface glycoprotein, hemagglutinin.</p>
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<affiliations><list><country><li>États-Unis</li>
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<region><li>Illinois</li>
</region>
<settlement><li>Chicago</li>
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<orgName><li>Université de l'Illinois à Chicago</li>
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<tree><country name="États-Unis"><region name="Illinois"><name sortKey="Rumschlag Booms, Emily" sort="Rumschlag Booms, Emily" uniqKey="Rumschlag Booms E" first="Emily" last="Rumschlag-Booms">Emily Rumschlag-Booms</name>
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<name sortKey="Rong, Lijun" sort="Rong, Lijun" uniqKey="Rong L" first="Lijun" last="Rong">Lijun Rong</name>
</country>
</tree>
</affiliations>
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