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ZNF16 inhibe la replicación de PEDV a través de la degradación de la proteína S1 mediada por la autofagia

Dongfang Zheng¹, Xinyu Yang², Wenzhen Qin²

¹College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, PR China; Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, PR China; Longhu Laboratory of Henan Province, Zhengzhou 450046, PR China.

Veterinary microbiology

|February 10, 2026

Resumen

La proteína 16 del dedo de zinc (ZNF16) inhibe el virus de la diarrea epidémica porcina (PEDV) mediante la degradación de su proteína S1. Esta nueva vía mediada por ZNF16 involucra a STUB1, Tollip y los lisosomas de autofagia, ofreciendo objetivos terapéuticos potenciales para PEDV.

Área de la Ciencia:

Virología Virología.
Biología Molecular Biología Molecular
Inmunología Inmunología.

Sus antecedentes:

El virus de la diarrea epidémica porcina (PEDV) causa pérdidas económicas significativas en la producción porcina debido a la diarrea severa en lechones.
Comprender las interacciones huésped-patógeno es clave para desarrollar vacunas y terapias efectivas contra el PEDV.

Objetivo del estudio:

Para investigar el papel de la proteína 16 del dedo de zinc (ZNF16) en la regulación de la replicación de PEDV.
Para dilucidar el mecanismo molecular por el cual ZNF16 afecta la proliferación de PEDV.

Principales métodos:

Pruebas basadas en células para evaluar la replicación del PEDV.
Western blotting y inmunoprecipitación para estudiar las interacciones de las proteínas.
Análisis de las vías de autofagia y lisosoma.

Principales resultados:

Se encontró que ZNF16 inhibe la proliferación de PEDV.
ZNF16 se dirige a la proteína PEDV S1 para su degradación a través de la vía de la autofagia-lisosoma.
ZNF16 recluta STUB1 y Tollip para facilitar la ubiquitinación de S1 y la posterior degradación lisosómica.

Conclusiones:

Se describe un nuevo mecanismo antiviral mediado por ZNF16 contra la PEDV.
El eje ZNF16-STUB1-Tollip-autolisosoma promueve la degradación de la proteína S1 viral, inhibiendo la replicación de la PEDV.
Esta vía representa un objetivo potencial para el desarrollo de nuevas intervenciones PEDV.

Palabras clave:

La autofagia es la autofagia.El PEDVV es el PEDVV.La proteína S1 es una proteína S1.El ZNF16 es el ZNF16.

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