| Literature DB >> 33082293 |
Ludovico Cantuti-Castelvetri1,2, Ravi Ojha3, Liliana D Pedro1,2, Minou Djannatian1,2, Jonas Franz4,5,6, Suvi Kuivanen7, Franziska van der Meer4, Katri Kallio3, Tuğberk Kaya1,2,8, Maria Anastasina3,9, Teemu Smura7, Lev Levanov7, Leonora Szirovicza7, Allan Tobi10, Hannimari Kallio-Kokko11, Pamela Österlund12, Merja Joensuu13, Frédéric A Meunier13, Sarah J Butcher3,9, Martin Sebastian Winkler14, Brit Mollenhauer15,16, Ari Helenius17, Ozgun Gokce8, Tambet Teesalu3,18,19, Jussi Hepojoki5,20, Olli Vapalahti7,11,21, Christine Stadelmann4, Giuseppe Balistreri22,23, Mikael Simons24,2,25.
Abstract
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.Entities:
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Year: 2020 PMID： 33082293 PMCID： PMC7857391 DOI： 10.1126/science.abd2985
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728