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An off-seasonal amantadine-resistant H3N2 influenza outbreak in Japan

Reiko Saito1, Danjuan Li, Chieko Shimomura

  • 1Department of Public Health, Graduate School of Medical and Dental Sciences, Niigata University, Japan. jasmine@med.niigata-u.ac.jp

The Tohoku Journal of Experimental Medicine
|September 9, 2006
PubMed

Insights

An off-season influenza outbreak in Nagasaki was caused by a novel amantadine-resistant H3N2 strain. This distinct clade N exhibited unique mutations, highlighting potential challenges for antiviral resistance surveillance.

Area of Science:

  • Virology
  • Epidemiology
  • Public Health

Background:

  • An unusual off-season influenza A H3N2 outbreak occurred in Nagasaki Prefecture, Japan, in September-October 2005.
  • This outbreak preceded the typical influenza season and was notable for a high prevalence of amantadine resistance.

Purpose of the Study:

  • To investigate the characteristics of the influenza A H3N2 strain responsible for the off-season outbreak.
  • To determine the genetic basis for amantadine resistance in the circulating strain.

Main Methods:

  • Rapid antigen testing was used for initial diagnosis of influenza-like illness (ILI).
  • Nasopharyngeal swabs from positive cases were used for virus isolation and genetic analysis.
  • Polymerase chain reaction (PCR) and gene sequencing were employed to identify specific mutations, including those in the M2 gene.
  • Phylogenetic analysis of the hemagglutinin (HA) gene was performed to compare the outbreak strain with contemporary H3N2 strains.

Main Results:

  • Influenza A was detected in 69.2% of tested ILI patients.
  • Amantadine resistance was confirmed through the detection of the S31N mutation in the M2 gene in all four analyzed samples.
  • Phylogenetic analysis revealed that the H3N2 strains formed a distinct cluster (clade N), differing from currently circulating strains due to dual mutations (S193F and D225N) in the HA gene.

Conclusions:

  • The off-season influenza outbreak was attributed to a distinct clade of H3N2 (clade N).
  • This clade possessed amantadine resistance due to the S31N mutation.
  • The findings underscore the emergence of drug-resistant influenza strains and the importance of molecular surveillance.

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