Role of vimentin in inhibiting akabane virus replication and its preliminary exploration of mechanisms involving autophagy and apoptosis

AKAV (Akabane virus), as a mosquito-borne virus, can cause abortions and stillbirths in pregnant ruminants, posing a threat to the global livestock industry. Vimentin (VIM), a key component of the IF cytoskeleton, plays a crucial role in viral infection by facilitating viral entry and modulating host antiviral responses. Dynamic changes in VIM transcription and protein expression levels were assessed longitudinally following infection and under varying multiplicities of infection using qRT-PCR and WB. The effects of VIM on viral replication were assessed in both VIM-overexpressing and knockout MA-104 cells through qRT-PCR, WB, TCID 50 , and IFA. Furthermore, VIM overexpression was combined with autophagy and apoptosis inhibitors to elucidate the association between VIM-mediated antiviral effects and autophagy/apoptosis-related pathways. Results showed that AKAV infection significantly upregulated the transcription of endogenous VIM in MA-104 cells, with the peak transcription level observed at a MOI of 3 and 60 h post-infection. Furthermore, in MA-104 cell models with VIM overexpression and knockout, it was found that VIM overexpression suppressed AKAV replication, while VIM knockout enhanced viral replication. Similarly, transient overexpression of bovine-derived VIM in MA-104 cells also inhibited AKAV replication. The combined application of autophagy and apoptosis inhibitors with VIM overexpression further enhanced the suppression of AKAV replication. This study elucidates the novel antiviral role of Vimentin against AKAV, providing a potential molecular target for developing strategies to control Akabane disease in livestock.