Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity.
Ludovico Cantuti-CastelvetriRavi OjhaLiliana D PedroMinou DjannatianJonas FranzSuvi KuivanenFranziska van der MeerKatri KallioTuğberk KayaMaria AnastasinaTeemu SmuraLev LevanovLeonora SziroviczaAllan TobiHannimari Kallio-KokkoPamela ÖsterlundMerja JoensuuFrédéric A MeunierSarah Jane ButcherMartin Sebastian WinklerBrit MollenhauerAri HeleniusOzgun GokceTambet TeesaluJussi M HepojokiOlli VapalahtiChristine StadelmannGiuseppe BalistreriMikael SimonsPublished in: Science (New York, N.Y.) (2020)
The causative agent of coronavirus disease 2019 (COVID-19) is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). For many viruses, tissue tropism is determined by the availability of virus receptors and entry cofactors on the surface of host cells. In this study, we found that neuropilin-1 (NRP1), known to bind furin-cleaved substrates, significantly potentiates SARS-CoV-2 infectivity, an effect blocked by a monoclonal blocking antibody against NRP1. A SARS-CoV-2 mutant with an altered furin cleavage site did not depend on NRP1 for infectivity. Pathological analysis of olfactory epithelium obtained from human COVID-19 autopsies revealed that SARS-CoV-2 infected NRP1-positive cells facing the nasal cavity. Our data provide insight into SARS-CoV-2 cell infectivity and define a potential target for antiviral intervention.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- induced apoptosis
- single cell
- randomized controlled trial
- cell cycle arrest
- endothelial cells
- cell therapy
- oxidative stress
- machine learning
- risk assessment
- bone marrow
- signaling pathway
- artificial intelligence
- mesenchymal stem cells
- big data
- cell proliferation
- disease virus