Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD, USA.
Autophagy. 2020 Dec;16(12):2131-2139. doi: 10.1080/15548627.2020.1817280. Epub 2020 Sep 23.
The COVID-19 pandemic, caused by the SARS-CoV-2 virus, is the most recent example of an emergent coronavirus that poses a significant threat to human health. Virus-host interactions play a major role in the viral life cycle and disease pathogenesis, and cellular pathways such as macroautophagy/autophagy prove to be either detrimental or beneficial to viral replication and maturation. Here, we describe the literature over the past twenty years describing autophagy-coronavirus interactions. There is evidence that many coronaviruses induce autophagy, although some of these viruses halt the progression of the pathway prior to autophagic degradation. In contrast, other coronaviruses usurp components of the autophagy pathway in a non-canonical fashion. Cataloging these virus-host interactions is crucial for understanding disease pathogenesis, especially with the global challenge of SARS-CoV-2 and COVID-19. With the recognition of autophagy inhibitors, including the controversial drug chloroquine, as possible treatments for COVID-19, understanding how autophagy affects the virus will be critical going forward. : 3-MA: 3-methyladenine (autophagy inhibitor); AKT/protein kinase B: AKT serine/threonine kinase; ATG: autophagy related; ATPase: adenosine triphosphatase; BMM: bone marrow macrophage; CGAS: cyclic GMP-AMP synthase; CHO: Chinese hamster ovary/cell line; CoV: coronaviruses; COVID-19: Coronavirus disease 2019; DMV: double-membrane vesicle; EAV: equine arteritis virus; EDEM1: ER degradation enhancing alpha-mannosidase like protein 1; ER: endoplasmic reticulum; ERAD: ER-associated degradation; GFP: green fluorescent protein; HCoV: human coronavirus; HIV: human immunodeficiency virus; HSV: herpes simplex virus; IBV: infectious bronchitis virus; IFN: interferon; LAMP1: lysosomal associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MCoV: mouse coronavirus; MERS-CoV: Middle East respiratory syndrome coronavirus; MHV: mouse hepatitis virus; NBR1: NBR1 autophagy cargo receptor; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2 (autophagy receptor that directs cargo to phagophores); nsp: non-structural protein; OS9: OS9 endoplasmic reticulum lectin; PEDV: porcine epidemic diarrhea virus; PtdIns3K: class III phosphatidylinositol 3-kinase; PLP: papain-like protease; pMEF: primary mouse embryonic fibroblasts; SARS-CoV: severe acute respiratory syndrome coronavirus; SKP2: S-phase kinase associated protein 2; SQSTM1: sequestosome 1; STING1: stimulator of interferon response cGAMP interactor 1; ULK1: unc-51 like autophagy activating kinase 1; Vps: vacuolar protein sorting.
由 SARS-CoV-2 病毒引起的 COVID-19 大流行是最近出现的一种对人类健康构成重大威胁的新兴冠状病毒。病毒-宿主相互作用在病毒生命周期和疾病发病机制中起着重要作用，细胞途径（如巨自噬/自噬）被证明对病毒复制和成熟既有不利影响也有有利影响。在这里，我们描述了过去 20 年描述自噬-冠状病毒相互作用的文献。有证据表明，许多冠状病毒会诱导自噬，尽管其中一些病毒会在自噬降解之前阻止途径的进展。相比之下，其他冠状病毒以非规范的方式篡夺自噬途径的成分。对这些病毒-宿主相互作用进行编目对于理解疾病发病机制至关重要，尤其是在 SARS-CoV-2 和 COVID-19 带来的全球挑战下。随着对自噬抑制剂（包括有争议的药物氯喹）作为 COVID-19 潜在治疗方法的认识，了解自噬如何影响病毒将是未来的关键。: 3-MA: 3-甲基腺嘌呤（自噬抑制剂）；AKT/protein kinase B: AKT 丝氨酸/苏氨酸激酶；ATG: autophagy related；ATPase: 三磷酸腺苷酶；BMM: 骨髓巨噬细胞；CGAS: 环状 GMP-AMP 合酶；CHO: 中国仓鼠卵巢/细胞系；CoV: coronaviruses；COVID-19: Coronavirus disease 2019；DMV: double-membrane vesicle；EAV: equine arteritis virus；EDEM1: ER degradation enhancing alpha-mannosidase like protein 1；ER: endoplasmic reticulum；ERAD: ER-associated degradation；GFP: green fluorescent protein；HCoV: human coronavirus；HIV: human immunodeficiency virus；HSV: herpes simplex virus；IBV: infectious bronchitis virus；IFN: interferon；LAMP1: lysosomal associated membrane protein 1；MAP1LC3/LC3: microtubule associated protein 1 light chain 3；MCoV: mouse coronavirus；MERS-CoV: Middle East respiratory syndrome coronavirus；MHV: mouse hepatitis virus；NBR1: NBR1 autophagy cargo receptor；CALCOCO2/NDP52: calcium binding and coiled-coil domain 2 (autophagy receptor that directs cargo to phagophores)；nsp: non-structural protein；OS9: OS9 endoplasmic reticulum lectin；PEDV: porcine epidemic diarrhea virus；PtdIns3K: class III phosphatidylinositol 3-kinase；PLP: papain-like protease；pMEF: primary mouse embryonic fibroblasts；SARS-CoV: severe acute respiratory syndrome coronavirus；SKP2: S-phase kinase associated protein 2；SQSTM1: sequestosome 1；STING1: stimulator of interferon response cGAMP interactor 1；ULK1: unc-51 like autophagy activating kinase 1；Vps: vacuolar protein sorting.
