自噬在小RNA病毒感染中的作用

The Autophagy in Picornavirus Infection

自噬是真核细胞所特有的一种高度保守的经溶酶体途径降解细胞内错误折叠或多余蛋白质、受损细胞器、胞内病原体的细胞代谢过程。小RNA病毒脱壳感染细胞时,快速激活自噬途径,诱导形成大量双层膜结构的自噬体。自噬能激活细胞表面的模式识别受体以及干扰素途径,增强组织相容性复合物对病毒抗原的提呈作用,发挥抑制小RNA病毒感染的天然免疫功能;此外,自噬体为小RNA病毒提供复制相关蛋白质和非细胞裂解性释放途径,促进感染细胞的胞内、胞外出现更多成熟的小RNA病毒粒子。该文对细胞自噬与小RNA病毒感染的研究概况与进展作一综述,为进一步开展解析不同小RNA病毒感染与自噬发生的时间、空间等的关系及阐明自噬作用于小RNA病毒感染的分子机制等研究提供参考。

Autophagy, a highly conserved lysosomal pathway in eukaryotic cells, is responsible for the degradation of intracellular misfolded or redundant proteins, damaged organelles and intracellular pathogens. The picornaviruses uncoating infection rapidly induces autophagy, which further activates the formation of substantial autophogosomes. Autophagy, as an innate antiviral immune pathway, can promote cell surface pattern recognition receptors and interferon pathway, and enhances presentation effect of major histocompatibility complex on virus antigens to inhibit picornavirus infection and replication. In addition, given that autophogosome provides picornavirus replication protease and autophagosome-mediated exit without lysis, autophagy can enhance intracellular and extracellular virus production via promoting picornavirus genome duplication and progeny virion release. This review concludes the role of autophagy on picornavirus replication, in order to support certain basis for analyzing the relationship between the infection of different picornavirus and the time and space of autophagy, and illustrating molecular mechanism of autophagy in picornavirus infection.