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Rumschlag-Booms E, Rong L. Influenza a virus entry: implications in virulence and future therapeutics. Adv Virol. 2013;2013:121924doi: 10.1155/2013/121924.
Rumschlag-Booms, E., & Rong, L. (2013). Influenza a virus entry: implications in virulence and future therapeutics. Advances in virology, 2013121924. https://doi.org/10.1155/2013/121924
Rumschlag-Booms, Emily, and Rong, Lijun. "Influenza a virus entry: implications in virulence and future therapeutics." Advances in virology vol. 2013 (2013): 121924. doi: https://doi.org/10.1155/2013/121924
Rumschlag-Booms E, Rong L. Influenza a virus entry: implications in virulence and future therapeutics. Adv Virol. 2013;2013:121924. doi: 10.1155/2013/121924. Epub 2013 Jan 09. PMID: 23365574; PMCID: PMC3556402.
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Adv Virol. 2013;2013:121924. doi: 10.1155/2013/121924. Epub 2013 Jan 09.

Influenza a virus entry: implications in virulence and future therapeutics.

Advances in virology

Emily Rumschlag-Booms, Lijun Rong

Affiliations

  1. Department of Biology, Northeastern Illinois University, Chicago, Chicago, IL 60625, USA.

PMID: 23365574 PMCID: PMC3556402 DOI: 10.1155/2013/121924

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.

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