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Cameron D Griffiths^1,2, Leanne M Bilawchuk^1,2, John E McDonough³

¹Li Ka Shing Institute of Virology, University of Alberta, Edmonton, Alberta, Canada.

|June 5, 2020

Resumen

El virus sincitial respiratorio (VSR) utiliza la nucleolina como un coreceptor para la entrada en las células. La inhibición de la proteína quinasa C zeta (PKCζ) bloquea el tráfico de nucleolina, reduciendo la replicación y la patología del RSV.

Área de la Ciencia:

Virología
Biología celular
Inmunología

Sus antecedentes:

La neumonía es una de las principales causas de muerte a nivel mundial, y el virus sincitial respiratorio (VSR) representa una carga significativa para la salud y tiene opciones terapéuticas limitadas.
El RSV infecta las células epiteliales ciliadas de las vías respiratorias, pero los mecanismos precisos de entrada del virus y las interacciones con los receptores siguen sin estar claros.
La nucleolina actúa como un coreceptor de entrada para el RSV y otros patógenos, facilitando la entrada celular.

Objetivo del estudio:

Para aclarar el mecanismo de entrada del RSV en las células huésped.
Identificar el papel de las vías de señalización celular específicas y los correceptores en la infección por el RSV.
Explorar objetivos terapéuticos potenciales para el RSV mediante la comprensión de su mecanismo de entrada.

Principales métodos:

Se investigó la entrada de RSV mediante el examen de la interacción entre la glicoproteína RSV-F y el receptor del factor de crecimiento similar a la insulina-1.
Estudió el papel de la señalización de la proteína quinasa C zeta (PKCζ) en el reclutamiento de la nucleolina a la membrana celular.
Se utilizaron cultivos de organoides de las vías respiratorias y modelos de ratones infectados por el RSV para evaluar el impacto de la inhibición de la activación de la PKCζ.

Principales resultados:

Se ha demostrado que la unión del RSV-F al receptor del factor de crecimiento parecido a la insulina-1 desencadena la activación de la PKCζ.
Se demostró que la señalización activada de PKCζ recluta nucleolina desde el núcleo hasta la membrana plasmática, donde se une a las partículas de RSV.
La inhibición de la activación de PKCζ impidió el tráfico de nucleolina a las partículas de RSV y redujo la replicación viral y la patología in vivo.

Conclusiones:

La entrada de RSV implica una cascada de señalización donde el compromiso del receptor conduce al reclutamiento de coreceptores a las partículas virales en la superficie celular.
La vía identificada que involucra a PKCζ y nucleolina representa un nuevo mecanismo de entrada viral.
Dirigirse a esta vía podría conducir al desarrollo de nuevas estrategias terapéuticas contra la infección por RSV.

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