Question & Answer

Q&A: What have we found out about the influenza A (H1N1) 2009 pandemic virus?

Stephen J Turner¹, Lorena E Brown¹, Peter C Doherty^1,2 and Anne Kelso³

¹  Department of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria 3010, Australia

²  Department of Immunology, St Jude Childrens Research Hospital, 332 Nth Lauderdale, Memphis, TN 38105, USA

³  WHO Collaborating Centre for Reference and Research on Influenza, 10 Wreckyn Street, North Melbourne, Victoria 3051, Australia

Journal of Biology 2009, 8:69doi:10.1186/jbiol179

Published:	18 September 2009

First paragraph (this article has no abstract)

It is not clear precisely what changes resulted in the increased severity of infection during the second wave of the 1918 Spanish influenza pandemic. Certainly the occurrence of multiple waves of influenza infection in the same year is unusual and one possibility is progressive adaptation of the 1918 Spanish influenza virus to its new human host [1]. Molecular analysis, for example, suggests that the virus that emerged during the second wave in the Northern hemisphere had undergone changes in the hemagglutinin (HA) binding site that increased binding specificity for human receptors [2]. This is presumed to have affected the replicative capacity and, therefore, the pathogenicity of the virus. The 1918 Spanish influenza virus also encoded a non-structural 1 (NS1) protein capable of blocking interferon production and thus prevention of viral replication by the host [3]. Changes in the NS1 protein may also have contributed to host adaptation and increased virulence [1]. Importantly, however, two of the features that account for the virulence of the highly pathogenic avian influenza A (H5N1) viruses are not present either in the Spanish influenza virus or in the current pandemic influenza A (H1N1) 2009 virus [4]. These are a lysine at position 627 of the polymerase basic subunit 2, and glutamic acid in position 92 of NS1 that, at least in animal models of infection, increase the replicative capacity of the virus and block host inhibition of viral replication, respectively [5,6].