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Originally published as JGV in Press, 10.1099/vir.2008.007260-0 on February 17, 2009 J Gen Virol 90 (2009), 900-908; 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

1 Institut für Virologie und Antivirale Therapie, Universitätsklinikum Jena, Hans Knöll Str. 2, D-07745 Jena, Germany
2 Friedrich Loeffler Institute, Federal Research Institute for Animal Health, Institute of Molecular Biology, Südufer 10, D-17493 Greifswald - Insel Riems, Germany
3 IDT Biologika GmbH, Bereich Forschung und Entwicklung, Am Pharmapark, D-06861 Dessau-Rosslau, Germany

Correspondence
Roland Zell
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 resistance 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.

Supplementary material is available with the online version of this paper.






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