Abstract
With the widespread use of a recently developed canine influenza virus (CIV) H3N8 vaccine, continual molecular evaluation of circulating CIVs is necessary for monitoring antigenic drift. The aim of this project was to further describe the genetic evolution of CIV, as well as determine any genetic variation within potential antigenic regions that might result in antigenic drift. To this end, the hemagglutinin gene of 19 CIV isolates from dogs residing in Colorado, New York, and South Carolina humane shelters was sequenced and compared to CIV strains isolated during 2003–2012. Phylogenetic analysis suggests that CIV might be diverging into two geographically distinct lineages. Using a mixed-effects model for evolution and single likelihood ancestor counting methods, several amino acid sites were found to be undergoing selection pressure. Additionally, a total of six amino acid changes were observed in two possible antigenic sites for CIVs isolated from Colorado and New York humane shelters between 2009 and 2011. As CIV isolates might be diverging into geographically distinct lineages, further experiments are warranted to determine the extent of antigenic drift occurring within circulating CIV.
Highlights
Serological evidence suggests H3N8 canine influenza virus (CIV) has been circulating in U.S dogs since as early as 1999 [1], it was not until 2004 that the virus was isolated from Florida racing greyhounds exhibiting signs of infectious respiratory disease [2]
These findings indicate that CIV continues to evolve from both its canine and equine influenza predecessors
All of the Colorado isolates were obtained in the first year of the study (2009–2010), while all of the New York viruses were from nasal swabs collected during study year two (2010–2011) (Table 2)
Summary
Serological evidence suggests H3N8 canine influenza virus (CIV) has been circulating in U.S dogs since as early as 1999 [1], it was not until 2004 that the virus was isolated from Florida racing greyhounds exhibiting signs of infectious respiratory disease [2]. CIV isolates sequenced between 2005 and 2008 share the same ten amino acid substitutions originally identified in early Florida CIV, as well as an additional nine amino acid substitutions among the influenza proteins [14] (three within the HA alone). These findings indicate that CIV continues to evolve from both its canine and equine influenza predecessors
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