PORCINE RESPIRATORY CORONAVIRUS-MEDIATED INTERFERENCE AGAINST INFLUENZA-VIRUS REPLICATION IN THE RESPIRATORY-TRACT OF FEEDER PIGS

Effect of prior porcine respiratory coronavirus (PRCV) infection on replication of H1N1-influenza virus in the respiratory tract of swine was studied. In an initial experiment, 3 groups of 5 feeder pigs were studied. Pigs of 2 groups were inoculated sequentially with PRCV, followed by H1N1-influenza virus at 2-and 3-day intervals. Pigs of the other group were inoculated with H1N1-influenza virus only. Pigs were monitored clinically and examined for nasal excretion of influenza virus. In the singly influenza virus-inoculated group, 83% of nasal swab specimens were influenza virus-positive over a period of 6 days after inoculation. In the dually virus-inoculated groups, only 27% (2-day interval) and 53% (3-day interval) of nasal swab specimens were virus-positive over the same postinoculation period. However, clinical signs of infection in these dually inoculated pigs were more severe than those in the singly influenza virus-inoculated pigs. There were no significant differences in antibody responses against influenza virus among the 3 groups of pigs. In a second experiment, 2 groups of pigs were studied. One group of pigs was inoculated sequentially with PRCV, followed by H1N1-influenza virus 2 days later; the other group was inoculated with H1N1-influenza virus only. Pigs of both groups were serially euthanatized on postinoculation days (PID) 1, 2, 3, and 4 (after influenza virus). At necropsy, influenza virus titer and immunofluorescence in lung tissue were determined and gross lung lesions were recorded. Influenza virus titer in the dually inoculated pigs (PID 1 and 2) was at least 100-fold reduced, compared with that in the corresponding singly inoculated pigs, and fluorescence was either not detected (PID 1) or was scant (PID 2). Differences in influenza virus replication between pigs of dually and singly inoculated groups became gradually less pronounced at PID 3 and 4. Lung lesions in the dually virus-inoculated pigs were distinctly more severe than those in the corresponding singly virus-inoculated pigs, and became progressively more pronounced as time after influenza virus inoculation progressed. These results indicate that PRCV infection may induce factors in the lungs that markedly interfere with replication and virus production during a subsequent influenza virus infection. On the other hand, clinical signs of infection and lung lesions were enhanced in the dually virus-inoculated pigs. It is believed that early nonspecific defense mechanisms in the lungs may have a role in the host antiviral response, as well as in development of lesions.