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Updated: Jul 30, 2025

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Published on: December 23, 2020
Endomembrane remodeling in SARS-CoV-2 infection
Di Chen1, Yan G Zhao2, Hong Zhang1,3
1National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks host endomembrane systems for viral entry, replication, and release. Targeting these host-pathogen interactions offers potential antiviral strategies against SARS-CoV-2.
Area of Science:
- Cell Biology
- Virology
- Molecular Biology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection involves intricate interactions between viral proteins and host cellular machinery.
- The endomembrane system, including the endoplasmic reticulum (ER) and Golgi apparatus, plays a critical role in the SARS-CoV-2 lifecycle.
- Understanding these host-pathogen interactions is crucial for developing effective antiviral therapies.
Purpose of the Study:
- To review how SARS-CoV-2 viral proteins remodel the host endomembrane system for viral entry, replication, assembly, and egress.
- To describe the hijacking of the host autophagic pathway by SARS-CoV-2 for viral production and immune evasion.
- To discuss potential antiviral therapies targeting the host cell endomembrane system.
Main Methods:
- This review synthesizes existing research on SARS-CoV-2 interactions with the host endomembrane system.
- It analyzes the molecular mechanisms by which viral proteins manipulate cellular compartments.
- The review also examines the role of autophagy in SARS-CoV-2 pathogenesis.
Main Results:
- SARS-CoV-2 utilizes endocytosis for entry, with endosomes fusing with lysosomes for S protein cleavage.
- Double-membrane vesicles derived from the ER serve as replication sites, and virions assemble at the ER-Golgi intermediate compartment.
- Viral proteins manipulate the endomembrane system for efficient replication, assembly, and release via secretory or lysosomal pathways.
Conclusions:
- SARS-CoV-2 extensively remodels the host endomembrane system to facilitate its lifecycle.
- Hijacking the autophagic pathway aids viral evasion and production.
- Targeting host-pathogen interactions within the endomembrane system presents a promising avenue for novel antiviral drug development.
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