Abstract
SUMOylation, a post-translational modification, is involved in interaction between hosts and viruses, and participates in diverse cellular processes including inflammatory responses and innate immunity. Here, we investigated the interaction between reovirus infection and the cellular SUMOylation machinery using grass carp reovirus (GCRV) as a model. Full-length cDNAs of grass carp SUMO-1 and SUMO-2 were obtained and phylogenetic analysis indicated that they shared high homology with those of higher vertebrates. The two modifiers and SUMO conjugating enzyme 9 (Ubc9) were ubiquitously expressed in all tested tissues of grass carp. During GCRV infection in CIK cells, transcriptional expressions of SUMO1/2 and Ubc9 were significantly inhibited; while UV-inactivated GCRV failed to inhibit the expression of the three molecules, which suggested that SUMOylation system was suppressed during viral replication. In CIK cells treated with inhibitor 2-D08 for SUMOylation, GCRV replication was not interfered; however, transcriptional analysis of immune genes involved in anti-viral interferon (IFN) response indicated that IRF2 and PKR were significantly up-regulated in CIK cells treated with inhibitor in contrast to IRF1, IRF7 and IFNI. Furthermore, 2-D08 treatment coupled with GCRV challenge resulted in higher IRF2 and PKR level during infection in comparison to those of CIK cells infected with GCRV only. These results indicated that inhibition of SUMOylation should result in the induction of PKR via IFN-independent manner, and both IFN-signaling and IFN-independent signaling seemed to involve in the upregulation of PKR during the process of GCRV infection. Repression of SUMOylation by GCRV might represent a cellular antiviral mechanism.