The rainbow trout (Oncorhynchus mykiss) interferon response in the ovary

Abstract

Immune responses in the ovary are tightly regulated to provide protection for the developing germ cells, which are very sensitive to inflammatory responses. This characteristic immune response is often used by viral pathogens to evade the immune system, replicate and be transmitted to other specimens through the ovary. Taking into account that in teleost fish, the innate immune system is considered crucial to the outcome of viral infections and the interferon (IFN) system is considered as the first line of defence against viruses, we have studied the IFN response in rainbow trout (Oncorhynchus mykiss) ovary using two viruses with different replicative capacity in this organ, namely viral haemorrhagic septicaemia virus (VHSV) and infectious pancreatic necrosis virus (IPNV). Both VHSV and IPNV are shed from the ovary, but while VHSV actively replicates at this site, IPNV remains silent. In this context, we have determined the levels of expression of IFNs and the IFN-induced Mx genes in the ovary upon in vivo and in vitro infections with VHSV and IPNV, and compared to the effects provoked by the viral mimic poly IC in vivo. We have demonstrated that while VHSV strongly up-regulates all the IFN genes studied, IPNV in vivo exposure either has no effect or even provokes strong suppression of IFN gene expression. These differences are not observed in vitro, even though IPNV does not replicate actively in this case either. Finally, to better understand the role that the production of type I IFN plays in the ovary, we have studied the effects of two type I recombinant rainbow trout IFNs (rtIFN1 and rtIFN2) to modulate both the expression of immune genes and to establish an antiviral state in the ovary. Interestingly, the ovary was able to respond to both rtIFN1 and 2, despite the fact that the IFN1 gene was not expressed here. Moreover, rtIFN1 and rtIFN2 not only modulated the expression of genes related to the IFN response, but also modulated inflammatory genes and significantly suppressed VHSV replication. © 2010 Elsevier Ltd.