Characterization of bovine kidney cells infected with lumpy skin disease virus.

Lumpy skin disease virus (LSDV) infection can cause systemic infection in cattle, accompanied by widespread viral dissemination in the skin, respiratory tract, lymphatic tissues, and visceral organs. However, the replication characteristics of the virus and the mechanisms by which it causes damage to host cells remain unclear. In this study, the ultrastructure of LSDV and the expression profile of host immune genes were investigated. The results showed that LSDV replicated efficiently in MDBK cells and induced cellular lesions, with the viral titer reaching approximately 1 × 10⁷ copies/mL. The assembly process of viral particles within cells and abnormal ultrastructure changes in organelles were observed by transmission electron microscopy. Transcriptomic analysis revealed that LSDV infection suppressed the host JAK-STAT pathway, while both the MAPK and systemic lupus erythematosus pathways were activated. These findings indicate a potentially paradoxical host response involving increased inflammatory signaling and attenuated antiviral immune responses, which may be associated with host cell damage. Our results have significant implications for elucidating the molecular mechanism of LSDV pathogenicity and provide important clues for the development of preventive and therapeutic strategies.