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El ARN subgenómico del dengue se une a TRIM25 para inhibir la expresión de interferón para la aptitud epidemiológica
Gayathri Manokaran1, Esteban Finol2, Chunling Wang3
1Program in Emerging Infectious Diseases, Duke-National University of Singapore Graduate Medical School, Singapore. Defence Medical and Environmental Research Institute, DSO National Laboratories, Singapore. Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Science (New York, N.Y.)
|July 4, 2015
Resumen
Una nueva cepa del virus del dengue (DENV) (PR-2B DENV-2) aumentó su potencial epidémico al producir más ARN del flavivirus subgenómico (ARNf). Este sfRNA elude la respuesta inmune del huésped, mejorando la aptitud viral.
Área de la Ciencia:
- Virología Virología.
- Inmunología Inmunología.
- Epidemiología La epidemiología.
Sus antecedentes:
- La propagación global del virus del dengue (DENV) ha llevado a un aumento de la diversidad genética, con algunas variantes que muestran un mayor potencial epidémico.
- Los mecanismos subyacentes a la aptitud viral en contextos epidemiológicos no se comprenden bien.
- Un clado específico de DENV de serotipo 2 (DENV-2) (PR-2B) surgió en Puerto Rico, reemplazando a un clado endémico (PR-1).
Objetivo del estudio:
- Para identificar los determinantes de la aptitud para el emergente PR-2B DENV-2 clade.
- Aclarar los mecanismos moleculares por los cuales PR-2B DENV-2 logra una mayor aptitud epidemiológica.
Principales métodos:
- Análisis comparativo de la replicación viral y la producción de ARN entre los clados PR-2B y PR-1 DENV-2.
- Investigación de las interacciones del ARN del flavivirus subgenómico (ARNf) con los factores inmunes del huésped.
- Evaluación del impacto de sfRNA en la expresión de interferón mediada por RIG-I.
Principales resultados:
- El clado PR-2B DENV-2 se replicó y produjo niveles significativamente más altos de ARN de flavivirus subgenómico (ARNf) en comparación con el ARN genómico en relación con el clado PR-1.
- El ARNf PR-2B demostró una unión dependiente de la secuencia al motivo tripartito 25 (TRIM25).
- Esta interacción inhibió la deubiquitilación mediada por TRIM25, crucial para las respuestas al interferón de tipo I inducidas por RIG-I.
Conclusiones:
- La producción mejorada de ARNf por PR-2B DENV-2 es un determinante clave de su mayor aptitud epidemiológica.
- El ARNf PR-2B facilita la evasión inmune viral al interferir con la vía TRIM25-RIG-I.
- Este estudio revela una nueva interacción entre el ARN viral y la proteína anfitriona que contribuye al potencial epidémico del virus del dengue.
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