First published September 2011, doi: 10.1128/JVI.05319-11 J. Virol. December 2011 vol. 85 no. 23 12742-12749
Antigenic and Genetic Evolution of Equine Influenza A (H3N8) Virus from 1968 to 2007?
N. S. Lewis1,2,3,*,
J. M. Daly2,?,
C. A. Russell1,4,
D. L. Horton1,3,6,
E. Skepner1,
N. A. Bryant2,
D. F. Burke1,
A. S. Rash2,
J. L. N. Wood3,
T. M. Chambers5,
R. A. M. Fouchier7,
J. A. Mumford3,
D. M. Elton2 and
D. J. Smith1,4,7
+ Author Affiliations
1Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, United Kingdom
2Animal Health Trust, Lanwades Park, Kentford, Newmarket CB8 7UU, United Kingdom
3Cambridge Infectious Diseases Consortium, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom
4Fogarty International Center, National Institutes of Health, 31 Center Drive?MSC 2220, Bethesda, Maryland 20892-2220
5Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, Kentucky 40546
6Wildlife Zoonoses and Vector Borne Diseases, Animal Health and Veterinary Laboratories Agency Weybridge, New Haw, Addlestone KT15 3NB, United Kingdom
7National Influenza Centre and Department of Virology, Erasmus Medical Centre, Dr. Molewaterplein 50, 3015GE Rotterdam, Netherlands
ABSTRACT
Equine influenza virus is a major respiratory pathogen in horses, and outbreaks of disease often lead to substantial disruption to and economic losses for equestrian industries. The hemagglutinin (HA) protein is of key importance in the control of equine influenza because HA is the primary target of the protective immune response and the main component of currently licensed influenza vaccines. However, the influenza virus HA protein changes over time, a process called antigenic drift, and vaccine strains must be updated to remain effective. Antigenic drift is assessed primarily by the hemagglutination inhibition (HI) assay. We have generated HI assay data for equine influenza A (H3N8) viruses isolated between 1968 and 2007 and have used antigenic cartography to quantify antigenic differences among the isolates. The antigenic evolution of equine influenza viruses during this period was clustered: from 1968 to 1988, all isolates formed a single antigenic cluster, which then split into two cocirculating clusters in 1989, and then a third cocirculating cluster appeared in 2003. Viruses from all three clusters were isolated in 2007. In one of the three clusters, we show evidence of antigenic drift away from the vaccine strain over time. We determined that a single amino acid substitution was likely responsible for the antigenic differences among clusters.
Antigenic and Genetic Evolution of Equine Influenza A (H3N8) Virus from 1968 to 2007?
N. S. Lewis1,2,3,*,
J. M. Daly2,?,
C. A. Russell1,4,
D. L. Horton1,3,6,
E. Skepner1,
N. A. Bryant2,
D. F. Burke1,
A. S. Rash2,
J. L. N. Wood3,
T. M. Chambers5,
R. A. M. Fouchier7,
J. A. Mumford3,
D. M. Elton2 and
D. J. Smith1,4,7
+ Author Affiliations
1Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, United Kingdom
2Animal Health Trust, Lanwades Park, Kentford, Newmarket CB8 7UU, United Kingdom
3Cambridge Infectious Diseases Consortium, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, United Kingdom
4Fogarty International Center, National Institutes of Health, 31 Center Drive?MSC 2220, Bethesda, Maryland 20892-2220
5Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, Kentucky 40546
6Wildlife Zoonoses and Vector Borne Diseases, Animal Health and Veterinary Laboratories Agency Weybridge, New Haw, Addlestone KT15 3NB, United Kingdom
7National Influenza Centre and Department of Virology, Erasmus Medical Centre, Dr. Molewaterplein 50, 3015GE Rotterdam, Netherlands
ABSTRACT
Equine influenza virus is a major respiratory pathogen in horses, and outbreaks of disease often lead to substantial disruption to and economic losses for equestrian industries. The hemagglutinin (HA) protein is of key importance in the control of equine influenza because HA is the primary target of the protective immune response and the main component of currently licensed influenza vaccines. However, the influenza virus HA protein changes over time, a process called antigenic drift, and vaccine strains must be updated to remain effective. Antigenic drift is assessed primarily by the hemagglutination inhibition (HI) assay. We have generated HI assay data for equine influenza A (H3N8) viruses isolated between 1968 and 2007 and have used antigenic cartography to quantify antigenic differences among the isolates. The antigenic evolution of equine influenza viruses during this period was clustered: from 1968 to 1988, all isolates formed a single antigenic cluster, which then split into two cocirculating clusters in 1989, and then a third cocirculating cluster appeared in 2003. Viruses from all three clusters were isolated in 2007. In one of the three clusters, we show evidence of antigenic drift away from the vaccine strain over time. We determined that a single amino acid substitution was likely responsible for the antigenic differences among clusters.