Porcine circovirus type 2 (PCV2) is an important pathogen in swine herds. We previously reported that glutamine (Gln) deficiency promoted PCV2 infection in vitro. Here, we established a Gln deficiency model in vivo and further investigated the detailed molecular mechanisms. In vivo and in vitro, Gln deficiency promoted PCV2 infection, which was evident through increased viral yields and PCV2 Cap protein synthesis. It also induced autophagy, as demonstrated by the increases in LC3-II conversion, SQSTM1 degradation, and GFP-LC3 dot accumulation. Autophagy inhibition abolished the effects of Gln deficiency on PCV2 infection. Inhibition of ROS generation alleviated the Gln deficiency-activated JAK2/STAT3 signaling pathway, thereby inhibiting autophagy induction. In vitro, the inhibition of STAT3 by an inhibitor or RNA interference blocked autophagy, thus reversing the effects of Gln deficiency on PCV2 infection. These results indicate that Gln deficiency activates autophagy by upregulating ROS-medicated JAK2/STAT3 signaling and thereby promoting PCV2 infection.

中文翻译：

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谷氨酰胺缺乏症通过激活ROS介导的ROS介导的JAK2 / STAT3信号通路自噬而促进PCV2感染。

猪圆环病毒2型（PCV2）是猪群中的重要病原体。我们先前曾报道谷氨酰胺（Gln）缺乏会在体外促进PCV2感染。在这里，我们建立了体内Gln缺乏症模型，并进一步研究了详细的分子机制。体内和体外Gln缺乏会促进PCV2感染，这可以通过增加病毒产量和PCV2 Cap蛋白合成来体现。它也诱导自噬，如LC3-II转化，SQSTM1降解和GFP-LC3点积累的增加所证明。自噬抑制作用消除了Gln缺乏对PCV2感染的影响。抑制ROS的产生减轻了Gln缺陷激活的JAK2 / STAT3信号通路，从而抑制了自噬的诱导。在体外，通过抑制剂或RNA干扰对STAT3的抑制作用阻止了自噬，从而逆转了Gln缺乏对PCV2感染的影响。这些结果表明，Gln缺乏症通过上调ROS介导的JAK2 / STAT3信号传导而激活自噬，从而促进PCV2感染。