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Canadian Journal of Infectious Diseases and Medical Microbiology
Volume 17, Issue 1, Pages 11-14
http://dx.doi.org/10.1155/2006/106989
Adult Infectious Disease Notes

Ode to Oseltamivir and Amantadine?

JM Conly1 and BL Johnston2

1Departments of Pathology and Laboratory Medicine, Medicine, and Microbiology and Infectious Diseases, Centre for Antimicrobial Resistance, University of Calgary, Calgary, Alberta, Canada
2Queen Elizabeth II Health Sciences Centre and Dalhousie University, Halifax, Nova Scotia, Canada

Received 30 January 2006; Accepted 30 January 2006

Copyright © 2006 Hindawi Publishing Corporation. 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.

Abstract

Influenza A and B viruses are the two major types of influenza viruses that cause human epidemic disease. Influenza A viruses are further categorized into subtypes based on two surface antigens: hemagglutinin (H) and neuraminidase (N). Influenza B viruses are not categorized into subtypes (1). Influenza A viruses are found in many animal species, including humans, ducks, chickens, pigs, whales, horses and seals, whereas influenza B viruses circulate only among humans. The H antigen contains common and strain-specific antigens, demonstrates antigenic variation, and acts as a site of attachment of the virus to host cells to initiate infection (1). The N antigen contains subtype-specific antigens and also demonstrates antigenic variation between subtypes. It is a surface glycoprotein possessing enzymatic activity essential for viral replication in both influenza A and B viruses. The N antigen allows the release of newly produced virions from infected host cells, prevents the formation of viral aggregates after release from the host cells, and prevents viral inactivation by respiratory mucous (2,3). It is thought that this enzyme may also promote viral penetration into respiratory epithelial cells and may contribute to the pathogenicity of the virus by promoting production of proinflammatory cytokines such as interleukin-1 and tumour necrosis factor from macrophages (4-6).