Viral entry into the host cell is the first step towards successful infection. Viral entry starts with virion attachment， and binding to receptors. Receptor binding viruses either directly release their genome into the cell， or enter cells through endocytosis. For DNA viruses and a few RNA viruses， the endocytosed viruses will transport from cytoplasm into the nucleus followed by gene expression. Receptors on the cell membrane play a crucial role in viral infection. Although several attachment factors， or candidate receptors， for the infection of white spot syndrome virus (WSSV) were identified in shrimp， the authentic entry receptors for WSSV infection and the intracellular signaling triggering by ... More
Viral entry into the host cell is the first step towards successful infection. Viral entry starts with virion attachment， and binding to receptors. Receptor binding viruses either directly release their genome into the cell， or enter cells through endocytosis. For DNA viruses and a few RNA viruses， the endocytosed viruses will transport from cytoplasm into the nucleus followed by gene expression. Receptors on the cell membrane play a crucial role in viral infection. Although several attachment factors， or candidate receptors， for the infection of white spot syndrome virus (WSSV) were identified in shrimp， the authentic entry receptors for WSSV infection and the intracellular signaling triggering by interaction of WSSV with receptors remain unclear. In the present study， a receptor for WSSV infection in kuruma shrimp， Marsupenaeus japonicus， was identified. It is a member of the immunoglobulin superfamily (IgSF) with a transmembrane region， and is similar to the vertebrate polymeric immunoglobulin receptor (pIgR); therefore， it was designated as a pIgR-like protein (MjpIgR for short). MjpIgR was detected in all tissues tested， and its expression was significantly induced by WSSV infection at the mRNA and protein levels. Knockdown of MjpIgR， and blocking MjpIgR with its antibody inhibited WSSV infection in shrimp and overexpression of MjpIgR facilitated the invasion of WSSV. Further analyses indicated that MjpIgR could independently render non-permissive cells susceptible to WSSV infection. The extracellular domain of MjpIgR interacts with envelope protein VP24 of WSSV and the intracellular domain interacts with calmodulin (MjCaM). MjpIgR was oligomerized and internalized following WSSV infection and the internalization was associated with endocytosis of WSSV. The viral internalization facilitating ability of MjpIgR could be blocked using chlorpromazine， an inhibitor of clathrin dependent endocytosis. Knockdown of Mjclathrin and its adaptor protein AP-2 also inhibited WSSV internalization. All the results indicated that MjpIgR-mediated WSSV endocytosis was clathrin dependent. The results suggested that MjpIgR is a WSSV receptor， and that WSSV enters shrimp cells via the pIgR-CaM-Clathrin endocytosis pathway.
