SCRV is a fatal pathogen to Siniperca chuats, Largemouth Bass, and can cause a high mortality rate [5]. SCRV is expected to be transmitted to and to cause disease in other species of fish by the transportation of infected fish[6].To date, there is no effective antiviral treatment against SCRV infection. A better understanding of the viral pathogenicity and pathology of the high-virulence Siniperca chuatsi rhabdovirus strains will be helpful to control the disease.
In the present study, two virulent Siniperca chuatsi rhabdovirus strains were used: SCRV-QY strain and SCRV-GM strain. SCRV-QY strain and SCRV-GM strain derived from Mandarin fish was pathogenic to Largemouth Bass. The SCRV-GM strain may be more virulent than the SCRV-QY strain, as there were more deaths in the group infected with the SCRV-GM strain. The clinical signs of disease among the fish included muscle hemorrhage, liver and spleen swelling or hemorrhage and even some skull deformation after infection with the SCRV-QY or SCRV-GM strains.
There were morphologic changes in the spleen, heart and intestine after infection [12]. Fishes infected with the SCRV-GM strain had more significant pathological changes than fishes infected with the SCRV-QY strain, possibly because the SCRV-GM strain was more virulent than the SCRV-QY strain. Moreover, the pathological changes were more serious on the seventh day after infection than on the fourteenth day after infection.
Attenuated virus strains replicate quickly and express large amounts of antigen protein, thereby inducing strong adaptive immune responses that result in rapid virus clearance. In contrast, pathogenic virus strains replicate at a lower rate than attenuated strains and can reach their target tissues [7]. In this study, the SCRV-GM strain may be more virulent than the SCRV-QY strain; thus, it could be detectable for a longer time, with more copies detected in the tissues by qRT-PCR. The brain, spleen, kidney may be the target organs, as they had higher viral RNA copy numbers. By the way, the brain had higher viral loads than other organs, which maybe suggest that the blood-brain barrier of fish is very different from that of other animals.
During the pathogen-host coevolution, many viruses have developed ways to evade the host innate immune responses, particularly the IFN pathways [8]. For example, the oldest and most famous rhabdovirus-rabies virus has selected mechanisms to hinder the host interferon response to sustain infection[9]. The P protein, one of the five rabies virus proteins, has been identified as a crucial factor for the inhibition of the IFN system[10].Moreover, attenuated rabies virus activate the innate immune responses, including the IFN pathway and inflammatory reactions, but the pathogenic rabies virus strain SHBRV induces very little or no inflammation and little or no up regulation of gene expression in the IFN and inflammatory pathways[11].In the present study, innate immune factors, such as interferon signaling genes (IRF-7), interferon effector genes (Mx), interleukin-1 receptor-associated kinase1 (IRAK-1) or antiviral responses, such as antiviral protein (viperin), were analyzed. However, none of them induce dupregulation of gene expression in the IFN and inflammatory pathways. It maybe that SCRV-QY and SCRV-GM strains were pathogenic and could inhibit the IFN and inflammatory pathways.