Oseltamivir- and Amantadine-Resistant Influenza Virus A (H1N1)

DOI: 10.3201/eid1601.091304
Suggested citation for this article: Cheng PKC, To APC, Leung TWC, Leung PCK, Lee CWC, Lim WWL. Oseltamivir- and amantadine-resistant influenza virus A (H1N1). Emerg Infect Dis. 2010 Jan; [Epub ahead of print]

Oseltamivir- and Amantadine-Resistant Influenza Virus A (H1N1)
To the Editor: We previously reported detection of double resistance to oseltamivir and amantadine of influenza virus A (H1N1) in Hong Kong during the first half of 2008 (1). Three different strains of A/Hong Kong/2652/2006-like (clade 2C) viruses that carried the S31N mutation in the matrix (M2) gene associated with amantadine resistance acquired a neuraminidase (NA) gene with CAT→TAT change at position 274 through either reassortment with an oseltamivir-resistant A/Brisbane/59/2007-like (clade 2B) virus or spontaneous H274Y mutation in the NA gene. A clade 2C strain resistant to both oseltamivir and amantadine also was detected in Cambodia in 2007 (2).

From July 2008 through December 2008, we continued to monitor antiviral susceptibility of all influenza A (H1N1) viruses in our laboratory, using previously described methods (1). Resistance to oseltamivir increased from 16.9% in July to 97.8% in December (Table). Sequencing of the hemagglutinin (HA) gene showed that, beginning in October, A/Brisbane/59/2007-like clade 2B virus had overtaken A/Hong Kong/2652/2006-like clade 2C virus to become the predominating circulating influenza A virus (H1N1) in Hong Kong. Of 916 isolates, 6 (0.7%), isolated from July through September 2008, were resistant to both amantadine and oseltamivir. Genetic analysis showed that 5 were similar to those we described previously, 4 were A/Hong Kong/2652/2006-like clade 2C viruses with spontaneous H274Y mutation in the NA gene, and 1 was a clade 2C virus but acquired a clade 2B NA gene carrying the H274Y mutation. The sixth double-resistant virus was an A/Brisbane/59/2007-like clade 2B virus with a spontaneous S31N mutation in the M2 gene. No epidemiologic link was detectable between these viruses. From October through December 2008, no double-resistant viruses were detected.
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