Autophagosome maturation stymied by SARS-CoV-2

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Abstract

Many pathogens are capable of disrupting autophagy within host cells. In this issue of Developmental Cell, Miao et al. discover that the SARS-CoV-2 protein ORF3a inhibits autophagosome-lysosome fusion by dysregulating the HOPS complex.

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Most cited references 10

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Autophagy in immunity and inflammation

Beth Levine, Noboru Mizushima, Herbert Virgin (2011)

Autophagy is an essential, homeostatic process by which cells break down their own components. Perhaps the most primordial function of this lysosomal degradation pathway is adaptation to nutrient deprivation. However, in complex multicellular organisms, the core molecular machinery of autophagy — the 'autophagy proteins' — orchestrates diverse aspects of cellular and organismal responses to other dangerous stimuli such as infection. Recent developments reveal a crucial role for the autophagy pathway and proteins in immunity and inflammation. They balance the beneficial and detrimental effects of immunity and inflammation, and thereby may protect against infectious, autoimmune and inflammatory diseases.

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Coronaviruses Hijack the LC3-I-Positive EDEMosomes, ER-Derived Vesicles Exporting Short-Lived ERAD Regulators, for Replication

Fulvio Reggiori, Iryna Monastyrska, Monique Verheije … (2010)

Summary Coronaviruses (CoV), including SARS and mouse hepatitis virus (MHV), are enveloped RNA viruses that induce formation of double-membrane vesicles (DMVs) and target their replication and transcription complexes (RTCs) on the DMV-limiting membranes. The DMV biogenesis has been connected with the early secretory pathway. CoV-induced DMVs, however, lack conventional endoplasmic reticulum (ER) or Golgi protein markers, leaving their membrane origins in question. We show that MHV co-opts the host cell machinery for COPII-independent vesicular ER export of a short-living regulator of ER-associated degradation (ERAD), EDEM1, to derive cellular membranes for replication. MHV infection causes accumulation of EDEM1 and OS-9, another short-living ER chaperone, in the DMVs. DMVs are coated with the nonlipidated LC3/Atg8 autophagy marker. Downregulation of LC3, but not inactivation of host cell autophagy, protects cells from CoV infection. Our study identifies the host cellular pathway hijacked for supplying CoV replication membranes and describes an autophagy-independent role for nonlipidated LC3-I.

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Genome-Scale Identification of SARS-CoV-2 and Pan-coronavirus Host Factor Networks

William M Schneider, Joseph M Luna, H.-Heinrich Hoffmann … (2020)

The coronavirus disease 2019 (COVID-19) pandemic has claimed the lives of over one million people worldwide. The causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a member of the Coronaviridae family of viruses that can cause respiratory infections of varying severity. The cellular host factors and pathways co-opted during SARS-CoV-2 and related coronavirus life cycles remain ill defined. To address this gap, we performed genome-scale CRISPR knockout screens during infection by SARS-CoV-2 and three seasonal coronaviruses (HCoV-OC43, HCoV-NL63, and HCoV-229E). These screens uncovered host factors and pathways with pan-coronavirus and virus-specific functional roles, including major dependency on glycosaminoglycan biosynthesis, sterol regulatory element-binding protein (SREBP) signaling, bone morphogenetic protein (BMP) signaling, and glycosylphosphatidylinositol biosynthesis, as well as a requirement for several poorly characterized proteins. We identified an absolute requirement for the VMP1, TMEM41, and TMEM64 (VTT) domain-containing protein transmembrane protein 41B (TMEM41B) for infection by SARS-CoV-2 and three seasonal coronaviruses. This human coronavirus host factor compendium represents a rich resource to develop new therapeutic strategies for acute COVID-19 and potential future coronavirus pandemics.

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Journal

Journal ID (nlm-ta): Dev Cell

Journal ID (iso-abbrev): Dev Cell

Title: Developmental Cell

Publisher: Elsevier Inc.

ISSN (Print): 1534-5807

ISSN (Electronic): 1878-1551

Publication date PMC-release: 22 February 2021

Publication date (Print): 22 February 2021

Publication date (Electronic): 22 February 2021

Volume: 56

Issue: 4

Pages: 400-402

Affiliations

[1 ]Department of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan

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Publisher Item ID: S1534-5807(21)00113-1

DOI: 10.1016/j.devcel.2021.02.002

PMC ID: 7898975

SO-VID: f1e45edb-a704-48ee-8d81-c7e364b86010

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Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

Autophagosome maturation stymied by SARS-CoV-2

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Novel Coronavirus Disease COVID-19

Most cited references 10

Autophagy in immunity and inflammation

Coronaviruses Hijack the LC3-I-Positive EDEMosomes, ER-Derived Vesicles Exporting Short-Lived ERAD Regulators, for Replication

Genome-Scale Identification of SARS-CoV-2 and Pan-coronavirus Host Factor Networks

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