Oseltamivir-Resistant Influenza A Pandemic (H1N1) 2009 Virus, Hong Kong, China

DOI: 10.3201/eid1512.091057
Suggested citation for this article: Chen H, Cheung CL, Tai H, Zhao P, Chan JFW, Cheng VCC, et al. Oseltamivir-resistant influenza A pandemic (H1N1) 2009 virus, Hong Kong, China. Emerg Infect Dis. 2009 Dec; [Epub ahead of print]

Oseltamivir-Resistant Influenza A Pandemic (H1N1) 2009 Virus, Hong Kong, China

Honglin Chen, Chung Lam Cheung, Hung Tai, Pengxi Zhao, Jasper F.W. Chan, Vincent C.C. Cheng, Kwok-Hung Chan, and Kwok-Yung Yuen

Author affiliation: The University of Hong Kong, Hong Kong Special Administrative Region, People’s Republic of China

Resistance to oseltamivir was observed in influenza A pandemic (H1N1) 2009 virus isolated from an untreated person in Hong Kong, China. Investigations showed a resistant virus with the neuraminidase (NA) 274Y genotype in quasi-species from a nasopharyngeal aspirate. Monitoring for the naturally occurring NA 274Y mutation in this virus is necessary.

Emergence of influenza A pandemic (H1N1) 2009 virus, presumably from swine to humans, has spread globally since April 2009 (1–3). This emergence prompted the World Health Organization to declare a pandemic caused by this virus on June 11, 2009. Although most cases of infection are mild or asymptomatic, 1,462 fatal cases were reported to the World Health Organization as of August 6, 2009 (www.who.int/csr/don/2009_09_11/en/index.html).

Experimental evidence from animal models showed that this virus was able to replicate to high titers in the lungs of infected animals (4), unlike seasonal influenza viruses, which mainly infect the upper respiratory tract. Serologic studies found that antibodies induced by current seasonal influenza vaccines show little cross-reactivity to pandemic (H1N1) 2009 virus (5).

Therapeutic options are presently limited to 2 neuraminidase (NA) inhibitors, oseltamivir and zanamivir, because this virus has a swine-origin matrix 2 (M2) gene, which contains a mutation associated with resistance to M2 ion channel blockers amamtadine and rimamtadine.

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