Virus-induced glycolysis-mediated histone lactylation promotes virus infection in shrimp via the S6K2 pathway [CUT&Tag]
As non-cellular organisms, viruses need to infect living cells to survive themselves. The virus infection must alter the host metabolisms. However, the influence of the metabolites from the altered metabolisms of virus-infected host cells on virus-host interactions remains largely unclear. To address this issue, a crustacean shrimp was challenged with white spot syndrome virus (WSSV) in this study. The in vivo results presented that the WSSV infection enhanced shrimp glycolysis, leading to the accumulation of lactate. The lactate accumulation in turn promoted the site-specific histone lactylation (H3K18la and H4K12la). To explore which target genes are affected by H3K18la or H4K12la, at 48 hours after WSSV infection, the shrimp hemocytes were collected and performed genome-wide CUT&amp;Tag analysis to identify candidate genes regulated by H4K12la or H3K18la. Therefore, our findings contributed novel insights into the effects and the underlying mechanism of the virus-induced metabolites on the virus-host interactions, providing new targets for the control of virus infection.