CHANNEL CATFISH REOVIRUS (CRV) INHIBITS REPLICATION OF CHANNEL CATFISH HERPESVIRUS (CCV) BY 2 DISTINCT MECHANISMS - VIRAL INTERFERENCE AND INDUCTION OF AN ANTIVIRAL FACTOR

Catfish reovirus (CRV), a double-stranded RNA virus, inhibited channel catfish herpesvirus (CCV) replication by 2 different mechanisms: (1) directly as a consequence of its own replication, and (2) indirectly d ue to the induction of an anti-viral factor. In the former, prior infe ction with CRV significantly reduced subsequent CCV protein synthesis and virus yield. CRV-mediated interference was greatest when CRV infec tion preceded CCV infection by 16 h, and was least when cell cultures were simultaneoulsy infected with both viruses. In the latter case, in fection of channel catfish ovary (CCO) cultures with W-inactivated CRV resulted in the synthesis (or release) of an anti-viral factor. Cells producing the factor were protected from CCV infection, as were cells which had been treated with spent culture medium containing anti-vira l activity. Interestingly an anti-viral activity was constitutively pr esent in long-term cultures of catfish T cells and macrophages. Whethe r this factor and the one induced by UV-inactivated CRV are identical is not known, but analogy to mammalian systems suggests that the forme r may be similar to type II interferon, whereas the latter may be the piscine equivalent of type I interferon. These results suggest that UV -inactivated CRV may prove useful in the induction and characterizatio n of interferon-like anti-viral proteins in the channel catfish and th at long-term cultures of catfish T cells and monocytes may serve as a ready source of additional anti-viral factors.