Question & Answer
Q&A: What do we know about influenza and what can we do about it?
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* Corresponding author: Peter C Doherty pcd@unimelb.edu.au
1 Department of Microbiology and Immunology, The University of Melbourne, Victoria 3010, Australia
2 Department of Immunology, St Jude Children's Research Hospital, Memphis, TN 31805, USA
Journal of Biology 2009, 8:46 doi:10.1186/jbiol147
Published: 26 May 2009First paragraph (this article has no abstract)
The crucial genes are those encoding the two viral surface proteins hemagglutinin (H or HA) and neuraminidase (N or NA). The influenza A viruses [1] that infect mammals like us replicate principally in the epithelial cells of the airways. The HA facilitates viral entry by binding to sialic acid residues on the epithelial cell surface, while the NA functions to cleave such attachments, and so release new virus particles, or virions, both from the cell and from the slimy mucous that protects the lung and trachea. The new virions are then free to spread the infection, both from cell to cell and to other susceptible individuals. Antibodies that bind to either the HA or the NA and block their function effectively prevent (or terminate) the infectious process and thus provide protective immunity. The anti-influenza drugs zanamivir and oselatamivir (Relenza and Tamiflu) operate by blocking the NA active site and, as this was first characterized by the structural analysis of NA-antibody complexes, are among the earliest examples of rational drug design.