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Visualization of SARS-CoV-2 using Immuno RNA-Fluorescence In Situ Hybridization
Published on: December 23, 2020
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ARF6 is a host factor for SARS-CoV-2 infection in vitro
Biorxiv : the Preprint Server for Biology
|June 15, 2022
Summary
This study reveals that SARS-CoV-2 entry into cells via endocytosis depends on cholesterol and ADP-ribosylation factor 6 (ARF6). Inhibiting ARF6 significantly reduces viral loads, suggesting ARF6 as a potential antiviral target.
Area of Science:
- Virology
- Cell Biology
Background:
- Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) utilizes ACE2 and other factors for cell entry, primarily through plasma membrane fusion or endocytosis.
- While plasma membrane fusion mechanisms are well-studied, SARS-CoV-2 endocytic entry pathways remain less understood.
Approach:
- Investigated SARS-CoV-2 endocytic entry using cholesterol-dependent Huh-7 cells, resistant to TMPRSS2 inhibitors.
- Utilized CRISPR-Cas9 to delete ADP-ribosylation factor 6 (ARF6) and employed the ARF6 inhibitor NAV-2729 to assess its role in viral infection.
- Validated findings in Calu-3 cells and kidney organoids to evaluate physiological relevance.
Key Points:
- SARS-CoV-2 endocytic entry is cholesterol-dependent but dynamin-independent.
- ADP-ribosylation factor 6 (ARF6) is crucial for SARS-CoV-2 uptake and infection in cell lines and organoid models.
- NAV-2729, an ARF6 inhibitor, demonstrated dose-dependent inhibition of SARS-CoV-2 infection.
Conclusions:
- ADP-ribosylation factor 6 (ARF6) plays a significant role in SARS-CoV-2 endocytic entry across various cellular contexts.
- Targeting ARF6 presents a promising strategy for developing novel antiviral therapies against SARS-CoV-2.
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