Antiviral responses of ATG13 to the infection of peste des petits ruminants virus through activation of interferon response
Antiviral responses of ATG13 to the infection of peste des petits ruminants virus through activation of interferon response
复制标题
ATG13 通过激活干扰素反应对小反刍兽疫病毒感染的抗病毒反应
DOI：
10.1016/j.gene.2020.144858
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发表时间：
2020-09-05
期刊：
影响因子：
3.5
通讯作者：
Ma, Xiao-xia
中科院分区：
文献类型：
--
作者：
Ma, Peng;Li, Lingxia;Ma, Xiao-xia
自噬相关（ATG）蛋白不仅是自噬机制的重要协调者，而且还调节许多其他细胞途径。在此，我们在细胞培养模型中证明ATG13对小反刍兽疫病毒（PPRV）的感染具有明显的抗病毒活性。我们发现PPRV感染或针对PPRV感染的干扰素（IFN）治疗显着诱导ATG13表达。从机制上讲，ATG13 刺激干扰素表达并随后激活 JAK-STAT 级联。这些激活触发了干扰素刺激基因（ISG）的转录，以发挥抗病毒活性。相反，ATG13 的缺失显着削弱了 RIG-IN 激活 IFN 反应的效力。总之，我们证明基础 ATG13 参与宿主针对 PPRV 感染的抗病毒活性，并且 ATG13 的过度表达激活 IFN 产生，以非常规方式抑制 PPRV 复制。
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.