J Gen Virol. 2009 Feb 17. [Epub ahead of print]
High prevalence of amantadine resistance among circulating European porcine influenza A viruses.
Krumbholz A, Schmidtke M, Bergmann S, Motzke S, Bauer K, Stech J, D?rrwald R, Wutzler P, Zell R. - Friedrich Schiller University;
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.
PMID: 19223487 [PubMed - as supplied by publisher]
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High prevalence of amantadine resistance among circulating European porcine influenza A viruses.
Krumbholz A, Schmidtke M, Bergmann S, Motzke S, Bauer K, Stech J, D?rrwald R, Wutzler P, Zell R. - Friedrich Schiller University;
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.
PMID: 19223487 [PubMed - as supplied by publisher]
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