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J Clin Virol. 2011 Jul;51(3):170-4. doi: 10.1016/j.jcv.2011.04.001. Epub 2011 May 11.

Genetic diversity and antiviral drug resistance of pandemic H1N1 2009 in Lebanon.

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  • 1Division of Virology, Department of Infectious Diseases, St Jude Children's Research Hospital, 262 Danny Thomas Place, Mail Stop 330, Memphis, TN 38105, USA. Hassan.Zaraket@stjude.org



In June 2009, the World Health Organization announced the 21st century's first influenza pandemic caused by pandemic influenza H1N1 2009 (H1N1 pdm).


Our goal was to analyze antiviral drug resistance and the phylogenetic relationships among hemagglutinin (HA) and neuraminidase (NA) genes of H1N1 pdm samples in Lebanon.


Nasopharyngeal swabs were collected from 197 patients with influenza-like illness from May 2009 through January 2010. Of the 50 influenza A-positive samples, 30 were analyzed for antiviral drug resistance by using in vitro susceptibility assays and cycling-probe real-time PCR. The HA and NA genes were also analyzed.


The results of hemagglutination-inhibition assays confirmed that all 30 analyzed samples were H1N1 pdm. In July 2009, community transmission of H1N1 pdm was detected in Lebanon, and an outbreak occurred in October 2009. The outbreak cases were caused by a strain with 4 mutations in the NA gene (i.e., V42I, N68T, N248D, and E462K) and 2 mutations in the HA gene: 1 in the Ca1 antigenic site (i.e., S206T) and 1 in the Ca2 antigenic site (i.e., D225E). This strain was closely related to a major H1N1 pdm cluster that was isolated worldwide. All 30 samples were amantadine-resistant, and none were zanamivir-resistant. The 1 oseltamivir-resistant sample appeared to be from a community-transmitted case in an otherwise healthy 2-year-old child.


Continuous monitoring of oseltamivir susceptibility among H1N1 pdm is essential to guide the effective use of this drug.

Copyright © 2011 Elsevier B.V. All rights reserved.

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