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MAVS forma agregados funcionales parecidos a priones para activar y propagar la respuesta inmune innata antiviral
Fajian Hou1, Lijun Sun, Hui Zheng
1Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.
Cell
|July 26, 2011
Resumen
La infección viral desencadena helicasas similares a RIG-I para activar la agregación MAVS, formando estructuras similares a priones que propagan señales antivirales. Este mecanismo explica cómo los agregados MAVS activan IRF3 y amplifican la respuesta inmune.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología Molecular Biología Molecular
- Virología Virología.
Sus antecedentes:
- Las helicasas tipo RIG-I detectan el ARN viral, activando el MAVS para inducir interferones tipo I.
- La unión de RIG-I a las cadenas de poliubiquitina K63 es crucial para la activación de MAVS, pero el mecanismo sigue sin estar claro.
Objetivo del estudio:
- Para dilucidar el mecanismo de activación de MAVS en la señalización antiviral.
- Para investigar el papel de la agregación de MAVS en la activación de IRF3.
Principales métodos:
- Observación de la formación de agregados MAVS durante la infección viral.
- Estudios in vitro en los que se utilizó proteína MAVS recombinante para formar fibrillas.
- Análisis de la conversión de MAVS por fibrillas parecidas a priones en presencia de cadenas de ubiquitina K63.
Principales resultados:
- La infección viral induce grandes agregados MAVS que activan el IRF3.
- Las MAVS recombinantes forman fibrillas parecidas a priones que activan el IRF3.
- RIG-I, con cadenas de ubiquitina K63, convierte MAVS en agregados similares a priones en las mitocondrias.
Conclusiones:
- La activación de MAVS implica un interruptor conformacional parecido a un prión, que forma agregados que propagan la señal antiviral.
- Este mecanismo parecido a los priones amplifica la respuesta inmune innata a las infecciones virales.
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