Previous research found that ochratoxin A (OTA) could promote PCV2 replication by inducing autophagy. The aim of this study is to evaluate the effect of dietary amino acid derivative taurine on OTA-promoted PCV2 replication and explore the underlying mechanism. The results showed that taurine could inhibit OTA-promoted PCV2 replication in PK-15 cells. The effect of taurine could be mediated by its ability to attenuate ROS level and block OTA-promoted autophagy. Indeed, induction of autophagy by rapamycin could suppress the inhibitory effect of taurine on OTA-promoted PCV2 replication. Furthermore, taurine supplementation inhibited 5ʹAMP-activated protein kinase (AMPK) and activated mammalian target of rapamycin (mTOR). Activation of AMPK by acadesine (AICAR) could suppress the effect of taurine. In conclusion, taurine treatment suppresses autophagy by regulating the ROS/AMPK/mTOR signaling axis, thereby inhibiting OTA-promoted PCV2 replication. These findings provide the rationale for the use of taurine as an intervention against PCV2 infection.

先前的研究发现曲霉毒素A（OTA）可以通过诱导自噬来促进PCV2复制。这项研究的目的是评估饮食氨基酸衍生物牛磺酸对OTA促进PCV2复制的影响，并探讨其潜在机制。结果表明，牛磺酸可以抑制OTA促进的PCV2在PK-15细胞中的复制。牛磺酸的作用可以通过其减弱ROS水平和阻断OTA促进的自噬的能力来介导。实际上，雷帕霉素诱导的自噬可以抑制牛磺酸对OTA促进的PCV2复制的抑制作用。此外，牛磺酸补充抑制5ʹAMP激活的蛋白激酶（AMPK）和雷帕霉素（mTOR）的哺乳动物靶标。由Acadesine（AICAR）激活AMPK可以抑制牛磺酸的作用。综上所述，牛磺酸治疗通过调节ROS / AMPK / mTOR信号转导轴来抑制自噬，从而抑制OTA促进的PCV2复制。这些发现为使用牛磺酸作为抗PCV2感染的干预措施提供了理论依据。