Abstract
Coronavirus disease 2019 (COVID-19), caused by a new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has instantaneously emerged as a worldwide pandemic. However, humans encountered other coronaviruses in the past, and they caused a broad range of symptoms, from mild to life-threatening, depending on the virus and immunocompetence of the host. Most human coronaviruses interact with the proteins and/or double-membrane vesicles of autophagy, the membrane trafficking pathway that degrades and recycles the intracellular protein aggregates, organelles, and pathogens, including viruses. However, coronaviruses often neutralize and hijack this pathway to complete their life cycle. In this review, we discuss the interactions of human coronaviruses and autophagy, including recent data from SARS-CoV-2-related studies. Some of these interactions (for example, viral block of the autophagosome–lysosome fusion), while being conserved across multiple coronaviruses, are accomplished via different molecular mechanisms. Therefore, it is important to understand the molecular interplay between human coronaviruses and autophagy for developing efficient therapies against coronaviral diseases.
Highlights
Autophagy is a cytoplasmic membrane trafficking process, which was initially discovered as a recycling pathway for bulk cytosol and, later, for specific intracellular components [1]
Seven human coronaviruses have been discovered to date
Some of them (HCoV229E, Human coronaviruses (HCoV)-NL63, HCoV-OC43, and HCoV-HKU1) cause infection with mild symptoms, while others (SARS-CoV, severe acute respiratory syndrome (SARS)-CoV-2, and Middle East respiratory syndrome (MERS)-CoV) infect humans with more severe outcomes and can be life-threatening. Both mild and severe coronaviruses interact with autophagy, the conserved membrane trafficking pathway that operates in all eukaryotic cells and brings intracellular material from the cytoplasm to the lysosome for degradation and recycling
Summary
Autophagy is a cytoplasmic membrane trafficking process, which was initially discovered as a recycling pathway for bulk cytosol and, later, for specific intracellular components [1] It is essential for cells in periods of starvation and other stresses for degradation of misfolded and aggregated proteins [2], as well as damaged and surplus organelles [3]. The severity of COVID-19 in some patients resembles Middle East respiratory syndrome (MERS) caused by the related coronavirus, MERS-CoV [9] These large viruses, enveloped by a lipid bilayer, enter host cells via binding to the cell surface receptors [10]. We review known interactions of human coronaviruses with autophagy, a fascinating pathway that recycles intracellular material via the double-membrane vesicular intermediates
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