Ma Peng, Li Lingxia, Jin Li, Zhang Derong, Cao Xin, Guo Fucheng, Zhao Yongqing, Bai Jialing, Ma Zhongren, Shang Youjun, Ma Xiao-Xia
Biomedical Research Center, Northwest Minzu University, Lanzhou, China.
State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China.
Gene. 2020 Sep 5;754:144858. doi: 10.1016/j.gene.2020.144858. Epub 2020 Jun 9.
Not only are autophagy-related (ATG) proteins the essential orchestrators of the autophagy machinery, but also they regulate many other cellular pathways. Here, we demonstrated that ATG13 exerted an obviously antiviral activity against the infection of peste des petits ruminants virus (PPRV) in cell culture model. We found that PPRV infection or the treatment with interferon (IFN) against PPRV infection significantly induced ATG13 expression. Mechanistically, ATG13 stimulated interferon expression and the subsequent activation of the JAK-STAT cascade. These activations triggered the transcription of interferon-stimulated genes (ISGs) to exert antiviral activity. Conversely, the loss of ATG13 significantly attenuated the potency of RIG-IN in activating IFN responses. In summary, we have demonstrated that basal ATG13 was involved in host antiviral activities against PPRV infection and the over-expression of ATG13 activated IFN production to inhibit PPRV replication in an unconventional fashion.
自噬相关（ATG）蛋白不仅是自噬机制的关键协调者，还调控许多其他细胞通路。在此，我们证明了ATG13在细胞培养模型中对小反刍兽疫病毒（PPRV）感染具有明显的抗病毒活性。我们发现PPRV感染或用干扰素（IFN）处理以对抗PPRV感染均显著诱导ATG13表达。从机制上讲，ATG13刺激干扰素表达以及随后JAK-STAT级联反应的激活。这些激活触发干扰素刺激基因（ISG）的转录以发挥抗病毒活性。相反，ATG13的缺失显著减弱了RIG-IN激活IFN反应的能力。总之，我们证明了基础ATG13参与宿主针对PPRV感染的抗病毒活性，并且ATG13的过表达以非传统方式激活IFN产生以抑制PPRV复制。
