Caprine parainfluenza virus type 3 N protein promotes viral replication via inducing apoptosis

Caprine parainfluenza virus type 3 (CPIV3) is one of the most important viral respiratory pathogens of goat. Accumulating evidence demonstrates that apoptosis is a cellular mechanism for the host response to pathogens, and it participates in regulating viral replication. However, there is little study on CPIV3-induced host cells apoptosis. In this study, primary goat tracheal epithelial (GTE) cells were established as a cellular model that is permissive to CPIV3 infection. Then, we showed that CPIV3 infection induced apoptosis in GTE cells, as determined by morphological changes, flow cytometry and TUNEL assay. Moreover, Caspase activity and the expression of pro-apoptotic genes further suggested that CPIV3 induced apoptosis by activating both the intrinsic and extrinsic pathways. Mechanistically, the ability of CPIV3 to induce apoptosis was activated by N protein, and the viral protein increased CPIV3 replication through effecting apoptosis. Overall, our findings showed that GTE cells that will enable further analysis of CPIV3 infection and offers novel insights into the mechanisms of CPIV3induced apoptosis in host cells.

Automated summary

The study showed that CPIV3 infection induces apoptosis in GTE cells through activating both intrinsic and extrinsic pathways. This finding provides valuable insights into the mechanisms of CPIV3-induced apoptosis in host cells, allowing for further analysis of CPIV3 infection.