Spread of Canine Influenza A(H3N2) Virus, United States.
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ABSTRACT:
SUBMITTER: Voorhees IEH
PROVIDER: S-EPMC5708240 | biostudies-literature | 2017 Dec
REPOSITORIES: biostudies-literature
Publications
Spread of Canine Influenza A(H3N2) Virus, United States.
Voorhees Ian E H IEH Glaser Amy L AL Toohey-Kurth Kathy K Newbury Sandra S Dalziel Benjamin D BD Dubovi Edward J EJ Poulsen Keith K Leutenegger Christian C Willgert Katriina J E KJE Brisbane-Cohen Laura L Richardson-Lopez Jill J Holmes Edward C EC Parrish Colin R CR
Emerging infectious diseases 20171217 12
A canine influenza A(H3N2) virus emerged in the United States in February-March 2015, causing respiratory disease in dogs. The virus had previously been circulating among dogs in Asia, where it originated through the transfer of an avian-origin influenza virus around 2005 and continues to circulate. Sequence analysis suggests the US outbreak was initiated by a single introduction, in Chicago, of an H3N2 canine influenza virus circulating among dogs in South Korea in 2015. Despite local control m ...[more]
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Project description:H3N2 canine influenza viruses are prevalent in Asian and North American countries. During circulation of the viruses in dogs, these viruses are occasionally transmitted to cats. If this canine virus causes an epidemic in cats too, sporadic infections may occur in humans because of the close contact between these companion animals and humans, possibly triggering an emergence of mutant viruses with a pandemic potential. In this study, we aimed to gain an insight into the mutations responsible for inter-species transmission of H3N2 virus from dogs to cats. We found that feline CRFK cell-adapted viruses acquired several mutations in multiple genome segments. Among them, HA1-K299R, HA2-T107I, NA-L35R, and M2-W41C mutations individually increased virus growth in CRFK cells. With a combination of these mutations, virus growth further increased not only in CRFK cells but also in other feline fcwf-4 cells. Both HA1-K299R and HA2-T107I mutations increased thermal resistance of the viruses. In addition, HA2-T107I increased the pH requirement for membrane fusion. These findings suggest that the mutations, especially the two HA mutations, identified in this study, might be responsible for adaptation of H3N2 canine influenza viruses in cats.
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