Porcine Beclin1 facilitates the proliferation of porcine circovirus type 2 by augmenting autophagy in PK-15 cells.

Porcine circovirus type 2 (PCV2) is a significant immunosuppressive pathogen that poses a serious threat to the global swine industry. PCV2 infection often triggers secondary infections with multiple pathogens, making it crucial to elucidate its replication mechanisms for precise prevention and control. Numerous studies have demonstrated that autophagy plays a crucial role in viral infection. However, as the core regulator of autophagy, it has remained unclear whether Beclin1 is involved in the replication of PCV2. In this study, we utilized PK-15 cells as a model to investigate the role of Beclin1-mediated autophagy in PCV2 proliferation. The results showed that PCV2 infection significantly induced autophagy. Knockdown of Beclin1 simultaneously suppressed autophagic activity and viral proliferation, whereas overexpression of Beclin1 markedly enhanced autophagy and increased viral proliferation. Pharmacological experiments further confirmed that the autophagy inducer rapamycin amplified Beclin1-mediated autophagy and promoted viral proliferation, whereas the autophagy inhibitor MHY1485 exerted the opposite effect. In summary, this study reveals a novel function of Beclin1 in positively regulating PCV2 proliferation by enhancing autophagic activity in PK-15 cells, providing a theoretical basis for targeting the autophagy pathway to develop strategies for PCV2 control.