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Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity.
Ludovico Cantuti-Castelvetri1,2, Ravi Ojha3, Liliana D Pedro1,2
1Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany.
Science (New York, N.Y.)
|October 21, 2020
Summary
Neuropilin-1 (NRP1) significantly enhances severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectivity by binding to its furin cleavage site. Blocking NRP1 or altering the cleavage site reduces viral entry, offering potential antiviral strategies.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19.
- Viral tissue tropism is often dictated by host cell surface receptors and entry cofactors.
- Understanding SARS-CoV-2 entry mechanisms is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the role of neuropilin-1 (NRP1) in SARS-CoV-2 cell entry and infectivity.
- To identify potential host targets for blocking SARS-CoV-2 infection.
Main Methods:
- Assessed the effect of NRP1 on SARS-CoV-2 infectivity.
- Utilized a monoclonal antibody to block NRP1.
- Created and tested a SARS-CoV-2 mutant with an altered furin cleavage site.
- Performed pathological analysis of human COVID-19 autopsy olfactory epithelium.
Main Results:
- Neuropilin-1 (NRP1) significantly potentiates SARS-CoV-2 infectivity.
- Monoclonal antibody blockade of NRP1 inhibited this potentiation.
- A SARS-CoV-2 mutant with an altered furin cleavage site showed reduced dependence on NRP1.
- SARS-CoV-2 was found to infect NRP1-positive cells in the human olfactory epithelium.
Conclusions:
- NRP1 is a key factor potentiating SARS-CoV-2 infectivity, particularly through its interaction with the viral furin cleavage site.
- NRP1-positive cells in the olfactory epithelium are infected by SARS-CoV-2.
- NRP1 represents a promising target for antiviral therapies against COVID-19.
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