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Editorial
March 11, 2009

The Evolution of Influenza Resistance and Treatment

Author Affiliations

Author Affiliations: Department of Medical Oncology, Dana-Farber Cancer Institute (Dr Weinstock); Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital (Dr Zuccotti); and Harvard Medical School (Drs Weinstock and Zuccotti), Boston, Massachusetts. Dr Zuccotti is Contributing Editor, JAMA, Chicago, Illinois.

JAMA. 2009;301(10):1066-1069. doi:10.1001/jama.2009.324

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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