FIG. 11.

Tentative model of H-1PV cytotoxicity. After parvovirus infection, expression of NS1 triggers an oxidative stress with accumulation of intracellular ROS associated with DNA damage. As a consequence of DNA damage, cells accumulate in G₂ phase and then undergo apoptosis and ultimately lysis. NS1 may also induce DNA damage by directly nicking DNA, thereby contributing to the cell cycle arrest. Furthermore, ROS may also be produced during the execution of the apoptotic pathway, reinforcing the cytotoxic activity of the virus.