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La neuropilina-1 es un factor huésped para la infección por SARS-CoV-2

James L Daly¹, Boris Simonetti², Katja Klein³

¹School of Biochemistry, Faculty of Life Sciences, Biomedical Sciences Building, University of Bristol, Bristol BS8 1TD, UK.

Science (New York, N.Y.)

|October 21, 2020

Resumen

La proteína del pico del SARS-CoV-2 se une a los receptores de la célula huésped a través de un motivo CendR. Esta interacción con la neuropilina-1 (NRP1) es crucial para la entrada del virus, lo que sugiere que la NRP1 es un objetivo terapéutico potencial para el COVID-19.

Área de la Ciencia:

Virología
Biología molecular
Biología celular

Sus antecedentes:

El coronavirus 2 del síndrome respiratorio agudo severo (SARS-CoV-2) es la causa de la COVID-19.
La proteína del pico viral (S) media la adhesión y la entrada de la célula huésped.
La proteasa huésped furin divide la proteína S en subunidades S1 y S2.

Objetivo del estudio:

Investigar la interacción entre la subunidad S1 del SARS-CoV-2 y los receptores de las células huésped.
Determinar el papel de la neuropilina-1 (NRP1) y NRP2 en la infección por el SARS-CoV-2.

Principales métodos:

Cristalografía de rayos X para visualizar el motivo S1 CendR que se une a NRP1.
Pruebas bioquímicas para confirmar la interacción.
Interferencia de ARN y inhibidores selectivos para bloquear la interacción.
Experimentos de cultivo celular para evaluar la entrada del virus y la infectividad.

Principales resultados:

El motivo S1 CendR se une directamente al receptor NRP1.
El bloqueo de la interacción S1-NRP1 redujo la entrada de SARS-CoV-2 y la infectividad en el cultivo celular.
El NRP1 actúa como un factor huésped que facilita la infección por SARS-CoV-2.

Conclusiones:

La neuropilina-1 (NRP1) es un factor huésped crítico para la infección por SARS-CoV-2.
Dirigirse a la interacción S1-NRP1 puede ofrecer una estrategia terapéutica contra el COVID-19.

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