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Published on: February 9, 2014
Autophagy in severe acute respiratory syndrome coronavirus 2 infection
Di Chen1, Hong Zhang1,2
1National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Abstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) orchestrates host factors to remodel endomembrane compartments for various steps of the infection cycle. SARS-CoV-2 also intimately intersects with the catabolic autophagy pathway during infection. In response to virus infection, autophagy acts as an innate defensive system by delivering viral components/particles to lysosomes for degradation. Autophagy also elicits antiviral immune responses. SARS-CoV-2, like other positive-stranded RNA viruses, has evolved various mechanisms to escape autophagic destruction and to hijack the autophagic machinery for its own benefit. In this review, we will focus on how the interplay between SARS-CoV-2 viral proteins and autophagy promotes viral replication and transmission. We will also discuss the pathogenic effects of SARS-CoV-2-elicited autophagy dysregulation and pharmacological interventions targeting autophagy for COVID-19 treatment.
Insights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks the autophagy pathway, a cellular defense mechanism, to enhance its replication and spread. Understanding this interaction may lead to new COVID-19 treatments targeting autophagy.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection involves host cell endomembrane remodeling.
- Autophagy, a cellular degradation process, plays a dual role in antiviral defense and viral manipulation.
- SARS-CoV-2 interacts with autophagy, impacting viral replication and host immune responses.
Purpose of the Study:
- To review the intricate relationship between SARS-CoV-2 and autophagy.
- To elucidate how viral proteins modulate autophagy for replication and transmission.
- To discuss the pathological consequences of autophagy dysregulation and potential therapeutic strategies.
Main Methods:
- Literature review focusing on the interplay between SARS-CoV-2 and autophagy.
- Analysis of mechanisms by which SARS-CoV-2 evades or exploits autophagy.
- Examination of research on pharmacological interventions targeting autophagy for COVID-19.
Main Results:
- SARS-CoV-2 proteins actively manipulate the autophagy pathway to facilitate viral replication and spread.
- Dysregulation of autophagy by SARS-CoV-2 contributes to disease pathogenesis.
- Autophagy modulation presents a potential therapeutic avenue for COVID-19 treatment.
Conclusions:
- The interaction between SARS-CoV-2 and autophagy is critical for viral propagation and pathogenesis.
- Targeting autophagy pathways offers promising therapeutic strategies for managing COVID-19.
- Further research into SARS-CoV-2-autophagy interplay is essential for developing effective treatments.
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