Phylogenetic analyses indicate that canine influenza viruses (CIVs) (H3N8) evolved from contemporary equine influenza virus (EIV). Despite the genetic relatedness of EIV and CIV, recent evidence suggests that CIV is unable to infect, replicate, and spread among susceptible horses. To determine whether equine H3N8 viruses have equally lost the ability to infect, cause disease, and spread among dogs, we evaluated the infectivity and transmissibility of a recent Florida sublineage EIV isolate in dogs. Clinical signs, nasal virus shedding, and serological responses were monitored in dogs for 21 days after inoculation. Real-time reverse transcription-PCR and hemagglutination inhibition assays showed that both the viruses have maintained the ability to infect and replicate in dogs and result in seroconversion. Transmission of EIV from infected to sentinel dogs, however, was restricted. Furthermore, both CIV and EIV exhibited similar sialic acid-α2,3-gal receptor-binding preferences upon solid-phase binding assays. The results of the in vivo experiments reported here suggesting that dogs are susceptible to EIV and previous reports by members of our laboratory showing limited CIV infection in horses have been mirrored in CIV and EIV infections studies in primary canine and equine respiratory epithelial cells. 1. Introduction Due to the partial host range restriction of influenza A viruses, transmission of an influenza virus from one species to another is relatively rare. However, such cross-species transmission events do occur and have generated severe disease outbreaks in new host species. The 1918 “Spanish flu” is a classic example of cross-species transmission with devastating results, as the influenza virus involved with the pandemic was likely transmitted directly from birds to humans [1]. Therefore, understanding the molecular mechanisms that allow these viruses to cross the species barrier and adapt to new hosts is crucial for identifying influenza viruses that could potentially threaten both human and animal health. While evidence has accumulated over the years indicating contributions by all eight gene segments [2–10], the examination of the impact of individual viral proteins to host range restriction is complicated by several factors. For example, mutations often occur in multiple gene segments during the process of virus adaptation to a new species [5, 11–13], and, while some of these mutations may indeed reflect adaptation of the virus to the new host, others may be introduced in response to host immune pressure, or they might simply represent
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