Grass carp reovirus induces apoptosis and oxidative stress in grass carp (Ctenopharyngodon idellus) kidney cell line

• GCRV induced apoptosis in CIK cells.
• Activation of apoptosis was dependent on caspase pathway.
• The oxidative damage induced by GCRV was mostly related to the virus replication.

Grass carp hemorrhage is an acute contagious disease caused by grass carp reovirus (GCRV). The pathogenesis of GCRV and the relationship between GCRV and the host cells remain unclear. The aim of the present study was to investigate the relations among apoptosis, intracellular oxidative stress and virus replication in GCRV infected-cells. The results showed that GCRV induced activation of caspase proteases as early as 12 h, and reached maximum activities at 24 h or 48 h post-infection in a grass carp kidney cell line (CIK cells). Meanwhile, the levels of tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β) also were increased in GCRV-infected CIK cells and showed a statistically significant difference from 24 h to 96 h post-infection. The infection of GCRV caused the destruction of entire monolayer and the death of host cells. Accompanied by the infection, a severe oxidative stress occurred, which led to extensive loss of antioxidants and formation of lipid peroxidation after 48 h post-infection. These data suggested that the apoptosis which was triggered at an early stage (12–24 h) in the viral infection cycle, might be independent of virus replication, while the oxidative stress induced by GCRV was mostly related to the virus replication.