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La base estructural de la producción de ARN de flavivirus subgenómico patógeno (ARNf) es el ARNf
Erich G Chapman1, David A Costantino, Jennifer L Rabe
1Department of Biochemistry and Molecular Genetics, School of Medicine, University of Colorado Denver, Aurora, CO 80045, USA.
Science (New York, N.Y.)
|April 19, 2014
Resumen
Los flavivirus patógenos producen estructuras de ARN resistentes que evaden las defensas de las células huésped. Este estudio revela la estructura cristalina de este ARN, descubriendo un pliegue anilíneo único que inhibe la degradación viral y promueve la infección.
Área de la Ciencia:
- Virología Virología.
- Biología Molecular Biología Molecular
- Biología Estructural Biología estructural.
Sus antecedentes:
- Los flavivirus son amenazas significativas para la salud mundial.
- Los ARN flavivirales subgenómicos (ARNf) permiten la infección viral al resistir la degradación de la exonucleasa de la célula huésped.
- El mecanismo de la resistencia de sfRNA a la exonucleasa Xrn1 era previamente desconocido.
Objetivo del estudio:
- Para determinar la base estructural de la resistencia de Xrn1 en el ARN flaviviral.
- Para dilucidar el mecanismo por el cual los ARNf evitan la degradación de la célula huésped.
Principales métodos:
- Cristalografía de rayos X para determinar la estructura 3D de un ARN flaviviral resistente a Xrn1 completo.
- Análisis de nucleótidos conservados y topología del ARN.
- Análisis funcionales para evaluar el impacto de la alteración estructural en la formación de ARNf.
Principales resultados:
- La estructura cristalina revela un pliegue compacto de ARN con pseudonodos entrelazados.
- El ARN forma una conformación en forma de anillo, con su extremo 5 'enhebrado a través del anillo.
- Los nucleótidos conservados son críticos para mantener esta estructura específica.
- La alteración de esta estructura anula la formación de ARNf durante la infección.
Conclusiones:
- La formación de ARNf es dependiente de un pliegue de ARN específico y conservado.
- Esta estructura de ARN interactúa directamente con y inhibe la exonucleasa de la célula huésped Xrn1.1.
- La topología del ARN confunde la actividad de la helicasa Xrn1, evitando la degradación del ARN.
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