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October 4, 2006

Shift Shown in Influenza A Adamantane Resistance—Reply

Author Affiliations

Letters Section Editor: Robert M. Golub, MD, Senior Editor.

JAMA. 2006;296(13):1585-1587. doi:10.1001/jama.296.13.1586

In Reply: We agree with Dr Shea and Dr Shah that explanations for the rapid increase in resistance to the adamantane-class antivirals among influenza A viruses should be investigated. A single point mutation in the transmembrane region of the M2 gene can confer resistance to amantadine and rimantadine.1 Such an event may occur spontaneously or as a result of selective pressure from treatment with these drugs; we cannot determine the exact mechanism underlying the rapid increase in resistance among US isolates. Influenza A viruses isolated from several continents during recent influenza seasons contain the serine-to-asparagine change at amino acid 31 of the M2 protein that conferred adamantane resistance among A(H3N2) viruses isolated during the 2005-2006 North American influenza season; this antigenic variant was first isolated in East Asia during the 2004-2005 season, and its subsequent spread led the World Health Organization to recommend that A/Wisconsin/67/2005 be used as the H3N2 component of the Northern Hemisphere 2006-2007 influenza vaccines.2 It is unlikely that US patterns of antiviral use led to adamantane resistance; it is more likely that resistance emerged in East Asia in association with a specific influenza A(H3N2) antigenic variant that had a selective advantage, allowing it to spread widely.

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