Mindin Activates Autophagy for Lipid Utilization and Facilitates White Spot Syndrome Virus Infection in Shrimp

Mindin is a secreted extracellular matrix protein that is involved in regulating cellular events through interacting with integrin. Studies have demonstrated its role in host immunity, including phagocytosis, cell migration, and cytokine production. However, the function of Mindin in the host-virus interaction is largely unknown. In the present study, we report that Mindin facilitates virus infection by activating lipid utilization in an arthropod, kuruma shrimp (Marsupenaeus japonicus). Shrimp Mindin facilitates white spot syndrome virus infection by facilitating viral entry and replication. By activating autophagy, Mindin induces lipid droplet consumption, the hydrolysis of triglycerides into free fatty acids, and ATP production, ultimately providing energy for virus infection. Moreover, integrin is essential for Mindin-mediated autophagy and lipid utilization. Therefore, by revealing the mechanism by which Mindin facilitates virus infection through regulating lipid metabolism, the present study reveals the significance of Mindin in the host-virus interaction. IMPORTANCE White spot syndrome virus (WSSV) is an enveloped double-stranded DNA virus that has had a serious influence on worldwide shrimp farming in the last 30 years. We have demonstrated that WSSV hijacks host autophagy and lipid metabolism for reproduction in kuruma shrimp (Marsupenaeus japonicus). These findings revealed the mechanism by which WSSV exploits host machinery for its infection and provided serial targets for WSSV prevention and control in shrimp farming.