Key result
PCV2 infection or Cap expression induces ORF3-independent apoptosis via PERK pathway activation and elevated ROS.
Why the study?
PCV2 infection triggers ER stress via PERK activation and increases cytosolic Ca2+ and ROS levels, but the mechanism of apoptosis induction independent of ORF3 was unclear.
The study demonstrates that PCV2 induces apoptosis independently of ORF3 through PERK pathway activation and calcium/ROS elevation.
PCV2 or Cap induces ORF3-independent apoptosis via Ca2+ and ROS; leaves open mechanistic roles and antiviral targets pending in vivo validation.
PCV2 encodes protein ORF3, a putative protein with proapoptotic activity. Our early studies showed that PCV2 infection triggers ER stress via selective activation of the PERK pathway, a branch of the ER stress pathways, in permissive cells for enhanced replication and infection increased cytosolic Ca 2+ and ROS levels. Here we clearly show that PCV2 infection or Cap expression induces ORF3-independent apoptosis via increased cytosolic and mitochondrial Ca 2+ levels and cellular ROS levels as a result of activation of the PERK pathway.
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Zhang et al. (2019) studied Porcine Circovirus Type 2 (PCV2) infection. PCV2 infection or Cap expression was evaluated on ORF3-independent apoptosis. PCV2 infection or Cap expression induces ORF3-independent apoptosis via increased cytosolic and mitochondrial Ca2+ levels and cellular ROS levels as a result of PERK pathway activation.
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