Reactive oxygen species regulate the replication of porcine circovirus type 2 via NF-κB pathway.

Intracellular redox state has been suggested to have various effects on the replication of different viruses within host cells. The aim of the present study was to investigate the influence of reactive oxygen species (ROS) on replication of porcine circovirus type 2 (PCV2), in PK15 cells. Following PCV2 infection there was a time-dependent increase in ROS. Antioxidant N-acetyl-l-cysteine treatment of cells resulted in lower ROS levels and lower PCV2 replication. In contrast, treatment by buthionine sulfoximine (BSO), a GSH synthesis inhibitor, resulted in elevation of ROS levels and increased PCV2 replication. Furthermore, inhibiting the activity of NF-κB, a redox-responsive transcription factor, suppressed BSO-mediated increase of PCV2 replication, indicating that increased PCV2 replication likely occurs via ROS activation of NF-κB. Taken together, our results indicate that the generation of ROS during PCV2 infection is involved in its replication and this progression is associated with the alteration in NF-κB activity induced by ROS.