SAM disminuye la replicación de VHC mediante regulación de procesos celulares
Keywords:
VHC, SAM, GSH, proteasoma, Estrés oxidativoAbstract
El agente etiológico de la hepatitis C crónica es el VHC, el cual es un virus que desencadena estrés oxidativo celular; sin embargo, el mecanismo involucrado es desconocido. En este trabajo se encontró que s-adenosil metionina (SAM) inhibe la replicación del VHC a nivel transcripcional y traduccional a una dosis de 1mM durante 24-72 h. Se demostró que SAM es capaz de modular negativamente la actividad de quimotripsina del proteasoma y el efecto se potencia al combinar un inhibidor del proteasoma (MG132) con SAM. Además, la adición de SAM estimula la biosíntesis de GSH en el contexto de la infección por VHC.
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