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Advances in VirologyVolume 2013 2013, Article ID 121924, 9 pages

Review Article

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

Department of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, IL 60612, USA

Received 9 August 2012; Revised 9 December 2012; Accepted 23 December 2012

Academic Editor: Hector Aguilar-Carreno

Copyright © 2013 Emily Rumschlag-Booms and Lijun Rong. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.

Autor: Emily Rumschlag-Booms and Lijun Rong



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