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Una serpentina da forma al entorno extracelular para prevenir la maduración del virus de la influenza A
Meike Dittmann1, Hans-Heinrich Hoffmann1, Margaret A Scull1
1Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY 10065, USA.
Cell
|February 14, 2015
Resumen
Los genes estimulados por interferón (ISG, por sus siglas en inglés) proporcionan defensa antiviral. Este estudio identificó a SERPINE1 (PAI-1) como un ISG que inhibe el virus de la influenza A (IAV) al dirigirse a las proteasas extracelulares, reduciendo la infectividad viral.
Área de la Ciencia:
- Virología Virología.
- Inmunología Inmunología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- Los genes estimulados por interferón (ISG) son cruciales para la defensa antiviral.
- La mayoría de los ISG estudiados se dirigen a las primeras etapas intracelulares de la replicación viral.
- Los mecanismos de inhibición viral en etapas tardías siguen siendo menos comprendidos.
Objetivo del estudio:
- Para identificar los ISG que inhiben las etapas tardías de la infección por el virus de la influenza A (IAV) utilizando una pantalla basada en imágenes.
- Para dilucidar el mecanismo antiviral de SERPINE1 (que codifica el inhibidor del activador del plasminógeno 1, PAI-1).
Principales métodos:
- Cribado de alto contenido basado en imágenes para identificar ISG antivirales.
- Ensayos in vitro para evaluar el efecto de la PAI-1 en la infección por VAI.
- Análisis de los polimorfismos de SERPINE1 en la susceptibilidad humana al VAI.
Principales resultados:
- SERPINE1 (PAI-1) fue identificado como un ISG con actividad antiviral directa contra IAV.
- PAI-1 inhibe el IAV al dirigirse a las proteasas extracelulares de las vías respiratorias, evitando la escisión de la glicoproteína viral y reduciendo la infectividad del virus progenitor.
- La deficiencia parcial de PAI-1 debido a un polimorfismo de SERPINE1 aumentó la susceptibilidad in vitro al VAI.
Conclusiones:
- PAI-1 juega un papel importante en la restricción de la infección IAV in vivo.
- Dirigirse a las proteasas extracelulares para inhibir los procesos virales en etapa tardía es un mecanismo antiviral clave.
- SERPINE1 y PAI-1 son factores importantes en la respuesta del huésped al VAI.
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