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David M. Weinstock, MD; Gianna Zuccotti, MD

JAMA. 2009;301(10):1066-1069. Published online March 2, 2009 (doi:10.1001/jama.2009.324).

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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

At the time, it was confidently held that influenza was unlikely to develop similar resistance to neuraminidase inhibitors (oseltamivir and zanamivir), the second class of influenza-directed agents.^4-5 The neuraminidase inhibitors were designed with an understanding of the structural interaction between neuraminidase and its natural substrate sialic acid. Because these . . . [Full Text of this Article]

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.

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