Figure 5
Activation of DDR is essential for efficient PCV2 growth.
(A) Inhibition of DDR activation blocks PCV2 yield production. PCV2-infected PK15 cells 48 h after treatment with ATM kinase inhibitor (ATMi), ATM/ATR kinase inhibitor (ATM/ATRi), or DNA-PK inhibitor (DNA-PKi) were inoculated into PK15 monolayer cells and virus production was assayed by IFA under a microscope. Virus titers were expressed as TCID50 per milliliter and values are means ± SD of the results of three independent experiments. (B) Effect of DDR inactivation on PCV2 DNA replication. Supernatants of the PCV2-infected PK15 cells were performed by real-time PCR analysis after 48 h of treatment with these three inhibitors for amounts of PCV2 DNA load. Data for the PCV2-infected cells treated with the inhibitor are percentages of the value for the PCV2-infected untreated cells (means ± SD of values from three independent experiments). (C) Effect of DDR inactivation on PCV2 protein expression. The PCV2-infected PK15 cells were assayed by IFA after 48 h of treatment with these three inhibitors for amounts of PCV2 viral ORF1 synthesis. The amounts of PCV2 ORF1 protein expression are expressed as percentages of the ORF1-expressing signals in the PCV2-infected untreated cells. Data are means ± SD from three independent experiments. *P < 0.05 for a comparison of the PCV2-infected and PCV2-infected inhibitor-treated cells.
