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Editorial |

The Evolution of Influenza Resistance and Treatment

David M. Weinstock, MD; Gianna Zuccotti, MD
JAMA. 2009;301(10):1066-1069. doi:10.1001/jama.2009.324.
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In February 2006, the US Centers for Disease Control and Prevention (CDC) reported that 92.3% of the circulating influenza A(H3N2) at that time was resistant to the adamantanes (amantadine and ramantidine), 1 of 2 pharmacological classes available for the treatment of influenza.1 The resistant viruses harbored an S31N amino acid substitution in the influenza M2 protein that confers resistance but does not affect virulence. Although resistance to adamantanes increased to 14.5% in the prior year,2 the dramatic increase in 2005-2006 came as a shock to both the medical and scientific communities and the public.3

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Figure. Frequency of Resistance to Adamantane Among Influenza A(H1N1) Isolates and Oseltamivir Among Influenza A(H3N2) Isolates Submitted to the Centers for Disease Control and Prevention in the United States
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Frequency of resistance among isolates submitted to the US Centers for Disease Control and Prevention.1,2,7,8,11,13 NA indicates not available. The number of H1N1 isolates tested for oseltamivir resistance in 2005-2006 and the number of adamantane resistant H3N2 isolates in 2006-2007 were not available. The oseltamivir resistance before the 2007-2008 influenza season was less than 1%.

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