Involvement of WSSV–shrimp homologs in WSSV infectivity in kuruma shrimp: Marsupenaeus japonicus

Abstract

White spot syndrome virus (WSSV) is pathogenic and specific to shrimp, and is capable of producing a persistent infection in the host. Moreover, shrimp are capable of persistently carrying a single or multiple viruses, allowing them to survive for long periods with latent infections. In order to identify genes that are specially involved in the intricate WSSV–shrimp association, we focused on homologs between the WSSV and shrimp genomes. We here investigated whether homologous WssvORFs ( WssvORF285, WssvORF332) and their homologs in the kuruma shrimp genome ( MjORF16, MjORF18) are important for WSSV infectivity by utilizing dsRNA-mediated RNA interference, and further proposed potential roles of homologous WssvORFs associated with the persistent viral infection stage. Homologous MjORFs were found to be highly up-regulated in several tested tissues upon WSSV infection. Injection of dsRNAs specific to homologous MjORFs, followed by WSSV challenge, led to reduced and delayed shrimp mortality when compared to that of shrimp without dsRNA injection. Silencing of homologous WssvORFs by specific dsRNAs sharply increased shrimp survival. WssvORF332 may function as a latency gene especially associated with the persistent WSSV infection stage while WssvORF285 may be classified into the same group as WssvVP28 and may play a role in virus penetration during the infection. Our results suggest that WSSV–shrimp homologs are involved in WSSV infectivity and support the hypothesis that homologous WssvORFs are related to WSSV latency and pathogenesis.