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Published online ahead of print on 17 February 2009 as doi:10.1099/vir.2008.007260-0
Journal of General Virology 2009;90:900.

A more recent version of this article appeared on April 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.2008.007260-0
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High prevalence of amantadine resistance among circulating European porcine influenza A viruses

Andi Krumbholz1, Michaela Schmidtke1, Silke Bergmann1, Susann Motzke1, Katja Bauer1, Jürgen Stech2, Ralf Dürrwald3, Peter Wutzler1 and Roland Zell1,4

1 Friedrich Schiller University;
2 Friedrich Loeffler Institute;
3 IDT Biologika GmbH

4 E-mail: roland.zell{at}med.uni-jena.de

Genetic analysis of the M2 sequence of European porcine influenza A viruses reveals a high prevalence of amantadine resistance due to the substitution of serine 31 by asparagine in all three circulating subtypes, H1N1, H3N2 and H1N2. The M segment of all resistant strains belongs to a single genetic lineage. Whereas the first amantadine-resistant porcine strain was isolated in 1989, isolation of the last amantadine-susceptible strain dates to 1987 suggesting a displacement of amantadine-susceptible viruses by resistant strains soon after emergence of the mutation. Analysis of natural selection by codon-based tests indicates negative selection of codons 30, 31 and 34 which confer amantadine resistance. The codons 2, 11-28 and 54 of porcine and human strains exhibit differences in the patterns of substitution rates suggesting different selection modes. Transfer of amantadine resistence by exchange of the M segment and viability of recombinant A/WSN/33 viruses with avian-like M segments raises concerns about the emergence of natural human reassortants.

Received 11 September 2008; accepted 30 November 2008.




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