Channel catfish reovirus (CRV) inhibits replication of channel catfish herpesvirus (CCV) by two distinct mechanisms:viral interference and induction of an anti-viral factor

Abstract

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 due to the induction of an anti-viral factor. In the former, prior infection with CRV significantly reduced subsequent CCV protein synthesis and virus yield. CRV-mediated interference was greatest when CRV infection preceded CCV infection by 16 h, and was least when cell cultures were simultaneoulsy infected with both viruses. In the latter case, infection of channel catfish ovary (CCO) cultures with UV-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-viral activity. Interestingly an anti-viral activity was constitutively present in long-term cultures of catfish T cells and macrophages. Whether this factor and the one induced by UV-inactivated CRV are identical is not known, but analogy to mammalian systems suggests that the former may be similar to type I1 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 characterization of interferon-like anti-viral proteins in the channel catfish and that long-term cultures of catfish T cells and monocytes may serve as a ready source of additional anti-viral factors.

Studies on Pathogenesis Following Single and Double Infection with Viral Hemorrhagic Septicemia Virus and Infectious Hematopoietic Necrosis Virus in Rainbow Trout (Oncorhynchus mykiss)

“…Double infection resulted in a more restricted distribution of IHN virus during the acute stage of the infection (days [3][4][5][6][7][8][9][10][11][12][13][14]. The statistical analysis of immunohistochemical findings showed significantly higher OR values for IHN-single compared with IHNdouble infected for all organs analyzed except spleen.…”

“…In vitro studies have shown that catfish reovirus inhibits replication of channel catfish herpesvirus, the mecha-nisms implicated being both interference and induction of interferon-like factors. 7 In vivo studies have been carried out on stocks of Atlantic salmon persistently infected with infectious pancreatic necrosis (IPN) virus. The study showed that, when these fish were infected with infectious salmon anemia virus, the IPN virus carrier stage was not activated.…”

Isolation and characterization of a rhabdovirus from co-infection of two viruses in mandarin fish

“…For example, Alonso et al (1999Alonso et al ( , 2003 demonstrated that IPNV interferes with the replication of IHNV in coinfection experiments of BF2 cells. Chinchar et al (1998) observed that channel catfish reovirus inhibits replication of channel catfish herpesvirus, and proposed possible mechanisms for both interference and induction of interferon-like factors. A more recent report on coinfection of two rhabdoviruses, viral hemorrhagic septicemia virus (VHSV) and IHNV, in rainbow trout supported the conclusion that viral co-infection results in some degree of interaction at the cell level, and thereby leads to a reduced systemic distribution of IHNV (Brudeseth et al, 2002).…”

Viral interference between infectious hypodermal and hematopoietic necrosis virus and white spot syndrome virus in Litopenaeus vannamei

“…This phenomenon likely involves viral interference, mediated either by intracellular process or by anti-viral molecules induced by IHHNV infection. Viral interference, in which one virus interferes with or induces resistance to subsequent infection by another virus, can be induced by a variety of mechanisms (Chinchar et al 1998, Youngner & Whitaker-Dowling 1999. For example, infection with one virus may block entry of another virus by down-regulating production of cellular receptors or through competition for a common receptor.…”