pDNAJB6 interaction with Cap promotes PCV2 replication through enhancing of autophagy. A Disruption of pDNAJB6/Cap interaction impedes PCV2 replication. PKpDNAJB6−/− cells (transfected pCI-pDNAJB6 or pCI-pDNAJB6ΔJ for 12 h), wild-type PK-15, and PKpDNAJB6−/− cells (transfected with pCI-neo (control)) were infected with PCV2 for 48 h, respectively. The relative production of progeny viruses was measured by TCID50 and calculated. **p < 0.01 versus wild-type PK-15 cells. ##p < 0.05 versus PKpDNAJB6−/− cells transfected with full-length pDNAJB6 expression plasmid. B, C The effects of an autophagy inhibitor on the production of progeny virions. After pretreatment with or without 3-MA (5 mM), cells were respectively transfected with the indicated plasmids, and then the cells were infected with PCV2 for 48 h. Relative viral production was measured and calculated. **p < 0.01 versus DMSO treated cells that transfected with same plasmid; ##p < 0.01 versus PKpDNAJB6−/− cells rescued wild-type pDNAJB6 with same treatment. &p < 0.05 versus wild-type PK-15 cells with same treatment. D, E Effect of atg5 silencing on the number of autophagosomes induced by PCV2 infection and progeny PCV2 production in cells infected with PCV2. The cells were transfected with control siRNA (siCtrl) and atg5 siRNA (siAtg5), then infected with PCV2. After infection with PCV2 for 24 h, the average number of green puncta was counted and calculated in 60 cells in each group (D). After infection with PCV2 for 48 h, the relative production of progeny virions was measured and calculated (E). Results are expressed as the mean ± SD (n = 3). **p < 0.01 versus the same type of cells transfected with siCtrl; #p < 0.05 versus wild-type PK-15 cells with the same treatment.