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.

► We investigate the influence of ROS on PCV2 replication in PK15 cells.
► PCV2 infection of PK15 cells induces ROS production.
► Reduction of ROS levels induced by NAC can decrease PCV2 replication.
► Elevation of ROS levels induced by BSO can increase PCV2 replication.
► Inhibition of NF-κB activation suppresses BSO-mediated increase in PCV2 replication.