Influenza viruses have continuously evolved into multiple mutant strains from several regions, resulting in aggravated endemic or epidemic outbreak conditions. In the 2000s, several outbreaks of inter-species transmission were reported, such as, the avian H3N2 influenza virus that crossed the host barrier to dogs. The inter-species transmission gave rise to the H3N2 canine influenza virus (CIV) that spread from East Asia to North America. The newly emerged H3N2 CIV was likely to infect to cats; however, ferrets, which had a SA receptor-binding pattern similar to that of humans, were not suitable natural hosts. In addition to avian-to-dog transmission, the infectivity of pdm H1N1 and seasonal H3N2 viruses in dogs was proven when artificial inoculation of the viruses with active viral shedding in dogs caused pathologic changes in the lungs. Studies on sero-prevalence and artificial infection suggested the possibility of co-infection of and reassortment between the two viruses in dogs; later, H3N1 and variants of M-variant H3N2 reassortants between pandemic H1N1/2009 and prototype H3N2 CIV were isolated. Notably, the H3N2 CIV with the matrix gene of the pdm H1N1 virus showed more efficient transmission in ferrets than the classic H3N2 CIV. These results implied that this primary companion animal, which lives in closer proximity to humans than pigs, might act as a mixing vessel or a source of novel influenza A virus in humans. Our findings emphasized the necessity of intensive monitoring for influenza infection in companion animals for investigating the potential for the emergence of novel human influenza strains.

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