Abstract
1 Department of Veterinary Hygiene and Microbiology, School of Veterinary Medicine, Hokkaido University, Sapporo 060
2 Department of Comparative Pathology, School of Veterinary Medicine, Hokkaido University, Sapporo 060, Japan
3 Department of Microbiology, University of Hong Kong, Pathology Building, Queen Mary Hospital Compound, Hong Kong
4 Department of Virology and Molecular Biology, St Jude Children's Research Hospital, 332 North Lauderdale, P.O. Box 318, Memphis, Tennessee 38101-0318
and5 Department of Pathology, University of Tennessee at Memphis, 800 North Madison Avenue, Memphis, Tennessee 38163, U.S.A.
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 virus in pigs. Of these, 38 were avian strains, including 27 with non-human-type haemagglutinins (HA; H4 to H13). At least one strain of each HA subtype replicated in the respiratory tract of pigs for 5 to 7 days to a level equivalent to that of swine and human viruses. These results indicate that avian influenza viruses with or without non-human-type HAs can be transmitted to pigs, thus raising the possibility of introduction of their genes into humans. Sera from pigs infected with avian viruses showed high titres of antibodies in ELISA and neutralization tests, but did not inhibit haemagglutination of homologous viruses, cautioning against the use of haemagglutination-inhibition tests to identify pigs infected with avian influenza viruses. Co-infection of pigs with a swine virus and with an avian virus unable to replicate in this animal generated reassortant viruses, whose polymerase and HA genes were entirely of avian origin, that could be passaged in pigs. This finding indicates that even avian viruses that do not replicate in pigs can contribute genes in the generation of reassortants.