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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 . . . [Full Text of this Article]

David K. Shay, MD, MPH
dshay@cdc.gov
Centers for Disease Control and Prevention
Atlanta, Ga

Rick A. Bright, PhD
Novavax, Inc
Malvern, Pa

Michael Shaw, PhD; Nancy J. Cox, PhD; Alexander I. Klimov, PhD
Centers for Disease Control and Prevention

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