CaMKIIγ-mediated vimentin structural rearrangement regulates FMDV replication.

FMDV infection induces rearrangement of host cell membrane structures and recruits various proteins to form a replication complex for viral replication. Vimentin, a major component of type III intermediate filaments, has been implicated in the replication processes of multiple viruses. This study identifies that Vimentin interacts with FMDV 2 C and participates in replication complex formation. Knockout of Vimentin significantly suppressed FMDV replication in BHK-21 cells. FMDV infection did not affect Vimentin expression but instead induced the rearrangement of Vimentin network structure. Treatment with IDPN and acrylamide disrupted Vimentin structural rearrangement and inhibited FMDV replication. Furthermore, we demonstrated that FMDV upregulates CaMKIIγ expression, which in turn promotes Vimentin phosphorylation at Ser39 and Ser83 to induce structural rearrangement. Inhibiting CaMKIIγ activity resulted in a significant reduction in FMDV replication. Overexpression of Vimentin effectively enhanced the replication of several RNA viruses, including Poliovirus type 1, Enterovirus 71, Respiratory enteric orphan virus type 3 strain 176, Coxsackievirus A16, and Human parainfluenza virus type 2. Our results indicate that Vimentin regulates the replication of multiple RNA viruses, providing a theoretical reference for in-depth investigation into the mechanisms of RNA virus infection and the development of antiviral drugs.