Identification of H2N3 influenza A viruses from swine in the United States

  1. Wenjun Ma*,,
  2. Amy L. Vincent,
  3. Marie R. Gramer,
  4. Christy B. Brockwell§,,
  5. Kelly M. Lager,
  6. Bruce H. Janke*,
  7. Phillip C. Gauger,
  8. Devi P. Patnayak,
  9. Richard J. Webby§, and
  10. Jürgen A. Richt,
  1. *Department of Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011;
  2. Virus and Prion Diseases of Livestock Research Unit, National Animal Disease Center, Agricultural Research Service, United States Department of Agriculture, Ames, IA 50010;
  3. Veterinary Diagnostic Laboratory, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108;
  4. §St. Jude Children's Research Hospital, Memphis, TN 38018; and
  5. Interdisciplinary Program, University of Tennessee Health Science Center, Memphis, TN 38163
  1. Communicated by Robert G. Webster, St. Jude Children's Research Hospital, Memphis, TN, October 31, 2007 (received for review August 30, 2007)

Abstract

Although viruses of each of the 16 influenza A HA subtypes are potential human pathogens, only viruses of the H1, H2, and H3 subtype are known to have been successfully established in humans. H2 influenza viruses have been absent from human circulation since 1968, and as such they pose a substantial human pandemic risk. In this report, we isolate and characterize genetically similar avian/swine virus reassortant H2N3 influenza A viruses isolated from diseased swine from two farms in the United States. These viruses contained leucine at position 226 of the H2 protein, which has been associated with increased binding affinity to the mammalian α2,6Gal-linked sialic acid virus receptor. Correspondingly, the H2N3 viruses were able to cause disease in experimentally infected swine and mice without prior adaptation. In addition, the swine H2N3 virus was infectious and highly transmissible in swine and ferrets. Taken together, these findings suggest that the H2N3 virus has undergone some adaptation to the mammalian host and that their spread should be very closely monitored.

Footnotes

  • To whom correspondence should be addressed at:
    National Animal Disease Center, 2300 Dayton Avenue, Ames, IA 50010.
    E-mail: juergen.richt{at}ars.usda.gov
  • Author contributions: W.M., A.L.V., K.M.L. and J.A.R. designed research; W.M., A.L.V., M.R.G., C.B.B., K.M.L., B.H.J., P.C.G., D.P.P., R.J.W. and J.A.R. performed research; W.M., A.L.V., M.R.G., K.M.L., B.H.J., R.J.W. and J.A.R. analyzed data; and W.M., A.L.V., M.R.G., K.M.L., R.J.W. and J.A.R. wrote the paper.

  • The authors declare no conflict of interest.

  • Data deposition: The sequences reported in this paper have been deposited in the GenBank database [accession nos. EU258935EU258942 (A/Sw/2124514) and EU258943EU258950 (A/Sw/4296424)].

  • This article contains supporting information online at www.pnas.org/cgi/content/full/0710286104/DC1.

« Previous | Next Article »Table of Contents