Arch Virol (2001) 146: 1063–1074
Diverged evolution of recent equine-2 inﬂuenza (H3N8)
viruses in the Western Hemisphere
A. C. K. Lai
, T. M. Chambers
, R. E. Holland, Jr.
, P. S. Morley
D. M. Haines
, H. G. G. Townsend
, and M. Barrandeguy
Department of Microbiology and Molecular Genetics, Oklahoma State University,
Stillwater, Oklahoma, U.S.A.
Department of Veterinary Science, Gluck Equine Research Center,
University of Kentucky, Lexington, Kentucky, U.S.A.
Department of Environmental Health, Colorado State University,
Fort Collins, Colorado, U.S.A.
Department of Veterinary Microbiology and Department of Large Animal Clinical
Sciences, Western College of Veterinary Medicine, University of Saskatchewan,
Saskatoon, Saskatchewan, Canada
Institute of Virology, CICV-INTA Castelar, Buenos Aires, Argentina
Accepted December 14, 2000
Summary. We reported previously that equine-2 inﬂuenza A virus (H3N8) had
evolved intotwogeneticallyandantigenically distinct“Eurasian” and “American”
lineages. Phylogenetic analysis, using the HA1 gene of more recent American
isolates, indicated a further divergence of these viruses into three evolution
lineages: A South American lineage, a Kentucky lineage, and a Florida lineage.
These multiple evolution pathways were not due to geographic barriers, as viruses
from different lineages co-circulated. For the Kentucky lineage, the evolution rate
was estimated to be 0.89 amino acid substitutions per year, which agreed with the
previously estimated rate of 0.8. For the South American lineage, the evolution
rate was estimated to be only 0.27 amino acid substitutions per year. This low
evolution rate was probably due to a unique alternating Ser138 to Ala138 sub-
stitutions at antigenic site A. For the Kentucky lineage, there was a preference
for sequential nonsynonymous substitutions at antigenic site B, which was also
a “hot spot” for amino acid substitutions. Convalescent sera had minimal cross-
reactivity to viruses of different lineages, indicating antigenic distinctions among
these viruses. In contrast to human H3N2 viruses, our results suggested that the
evolution of equine-2 inﬂuenza virus resembled the multiple evolution pathways
of inﬂuenza B virus.