Insights into the Antiviral Immunity against Grass Carp (Ctenopharyngodon idella) Reovirus (GCRV) in Grass Carp

Figure 1

Antiviral immune response of HMGBs induced by GCRV infection in CIK cells. GCRV infection induces diverse nucleocytoplasmic shuttling of grass carp HMGBs via two main methods: (1) upon GCRV infection, some HMGBs such as HMGB1a, HMGB1b, HMGB2b, and HMGB3a shuttle from nucleus to cytoplasm. Subsequently, a huge member of cells subject to apoptosis or karyotheca rupture, which result in cells death and passive release of HMGBs. On the other hand, some live cells can also actively secrete HMGBs to extracellular space; (2) even though GCRV fail to evoke nuclear exports of some HMGBs such as HMGB2a and HMGB3b, but the cells will undergo necrosis or damage. So those HMGBs are released to the extracellular matrix. Afterwards, the extracellular HMGBs initiate activation of TLRs- and RLRs-mediated antiviral immunity of neighboring cells.