Hokkaido University · Medicine
Professor Hiroshi Kida's research lab specializes in influenza virology, with a focus on the ecology, transmission, and molecular mechanisms of avian influenza viruses in natural hosts such as ducks and pigs. The lab investigates viral adaptation, host range, and the potential for genetic reassortment that could lead to pandemic strains, particularly examining how avian influenza viruses interact with mammalian hosts. Their work combines experimental virology, virological surveillance, and immunological analysis to understand the zoonotic potential of influenza A viruses.
Figures are computed from collected data and may differ slightly.
Pandemic strains of influenza A virus arise by genetic reassortment between avian and human viruses. Pigs have been suggested to generate such reassortants as intermediate hosts. In order for pigs to serve as 'mixing vessels' in genetic reassortment events, they must be susceptible to both human and avian influenza viruses. The ability of avian influenza viruses to replicate in pigs, however, has not been examined comprehensively. In this study, we assessed the growth potential of 42 strains of
Influenza viruses A/duck/Hokkaido/5/77 (Hav7N2), A/budgerigar/Hokkaido/1/77 (Hav4Nav1), A/Kumamoto/22/76 (H3N2), A/Aichi/2/68 (H3N2), and A/New Jersey/8/76 (Hsw1N1) were experimentally inoculated into Pekin ducks. Of these, the influenza viruses of duck and budgerigar origin replicated in the intestinal tract of the ducks. The infected ducks shed the virus in the feces to high titers, but did not show clinical signs of disease and scarcely produced detectable serum antibodies. Using immunofluore
Three influenza A viruses possessing hemagglutinin-Hav7 and neuraminidase-N2 were isolated from 20 wild free-flying ducks in Hokkaido, Japan in autumn, 1977. The neuraminidase antigen of these viruses cross-reacted with the Asian influenza virus (H2 N2) but reacted scarcely with the Hong Kong strain (H3 N2Y in cross neuraminidase-inhibition tests.
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