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Regulación de la expresión de Gag-Pol del VIH-1 por Shiftless, un inhibidor del desplazamiento del marco ribosomal

Xinlu Wang¹, Yifang Xuan¹, Yuling Han²

¹CAS Key Laboratory of Infection and Immunity, CAS Centre for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.

|January 26, 2019

Resumen

Shiftless (SFL) es un factor huésped recientemente identificado que inhibe el desplazamiento del marco ribosomal programado (-1PRF) en el VIH-1 y otros ARNm. La SFL se une al ARNm y a los ribosomas, causando la terminación prematura de la traducción y la inhibición de amplio espectro del PRF-1.

Área de la Ciencia:

Biología molecular
Virología
La genética

Sus antecedentes:

El desplazamiento del marco ribosómico programado -1 (-1PRF) es un mecanismo de recodificación de traducción crucial para la replicación viral, especialmente en la síntesis Gag-Pol del VIH-1.
El mantenimiento de la relación exacta de Gag a Gag-Pol es vital para la producción eficiente del VIH-1.

Objetivo del estudio:

Para identificar los factores del huésped que influyen en el cambio de marco ribosómico programado del VIH-1.
Caracterizar el mecanismo por el cual Shiftless (SFL) afecta al -1PRF.

Principales métodos:

Se investigó el papel del gen C19orf66 estimulado por el interferón (Shiftless) en el VIH-1 -1PRF.
Analizó la interacción de SFL con el ARNm viral y celular y los ribosomas de traducción.
Evaluó el impacto de SFL en la terminación de la traducción utilizando la regulación a la baja de los factores de liberación eRF3 y eRF1.

Principales resultados:

Shiftless (SFL) fue identificado como un factor anfitrión que inhibe el VIH-1 -1PRF.
SFL demostró una inhibición de amplio espectro de -1PRF a través de varios ARNm virales y celulares.
SFL se une a la señal -1PRF y al ribosoma, induciendo la terminación prematura de la traducción.
Los niveles reducidos de eRF3 o eRF1 disminuyeron la terminación prematura mediada por SFL.

Conclusiones:

La SFL actúa como un inhibidor de amplio espectro del desplazamiento del marco ribosómico programado.
La SFL interfiere con el proceso de desplazamiento del marco al unirse al ARNm y a los ribosomas, lo que lleva a la terminación prematura.
Estos hallazgos mejoran la comprensión de los mecanismos de -1PRF e identifican un nuevo factor de huésped involucrado en la regulación de la traducción.

Palabras clave:

No lo sé.El VIH-1 Factor antiviral del huésped Terminación prematura de la traducción Programación de desplazamiento de cuadro ribosomal Recodificación de la traducción

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