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Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity #MMPMID33082293
Cantuti-Castelvetri L; Ojha R; Pedro LD; Djannatian M; Franz J; Kuivanen S; van der Meer F; Kallio K; Kaya T; Anastasina M; Smura T; Levanov L; Szirovicza L; Tobi A; Kallio-Kokko H; Osterlund P; Joensuu M; Meunier FA; Butcher SJ; Winkler MS; Mollenhauer B; Helenius A; Gokce O; Teesalu T; Hepojoki J; Vapalahti O; Stadelmann C; Balistreri G; Simons M
Science 2020[Nov]; 370 (6518): 856-860 PMID33082293show ga
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.