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Polimorfismos de un solo aminoácido en STING modulan la evasión inmune y el espectro de patogenicidad del iridovirus

Xiaowei Qin^1,2, Mincong Liang¹, Weiqiang Pan¹

¹State Key Laboratory for Biocontrol & Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), Guangdong Province Key Laboratory for Aquatic Economic Animals, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, China.

Proceedings of the National Academy of Sciences of the United States of America

|January 23, 2026

Resumen

Los polimorfismos de un solo aminoácido en las proteínas del hospedador estimulador de genes de interferón (STING) pueden alterar la patogenicidad viral. Una variación específica de STING dicta si el virus de necrosis infecciosa del bazo y el riñón (ISKNV) puede evadir las respuestas inmunes y causar alta mortalidad.

Área de la Ciencia:

Virología
Inmunología
Biología Evolutiva

Sus antecedentes:

La coevolución huésped-virus impulsa la evasión inmune viral y la patogenicidad.
Los mecanismos subyacentes a los cambios en la patogenicidad viral entre especies no se comprenden completamente.

Objetivo del estudio:

Investigar el papel de los polimorfismos de un solo aminoácido (SAP) en el estimulador de genes de interferón (STING) del huésped en la modulación de la evasión inmune viral y la patogenicidad.
Determinar cómo ISKNV interactúa con STING de diferentes especies de peces.

Principales métodos:

Se identificaron residuos específicos en STING de pez mandarín a los que se dirige la proteína VP012R de ISKNV.
Se analizó el impacto de los polimorfismos de STING (K315/R315) en la evasión inmune viral y la patogenicidad.
Se realizó un análisis filogenético para correlacionar las variantes de STING con las tasas de mortalidad del huésped.

Principales resultados:

ISKNV VP012R se dirige a STING de pez mandarín en C196 y K315, promoviendo la degradación y suprimiendo las respuestas de interferón.
El polimorfismo K315/R315 de STING actúa como un interruptor molecular: K315 permite la evasión inmune viral y la degradación de STING en huéspedes susceptibles, mientras que R315 mantiene la estabilidad de STING en huéspedes resistentes.
El análisis filogenético reveló una correlación entre la variante K315 y una alta mortalidad del huésped (letalidad ≥50%), en comparación con la variante R315 en huéspedes resistentes (≤25% de letalidad).

Conclusiones:

Los SAP de proteínas del huésped pueden modular el espectro de patogenicidad de virus como ISKNV.
Los polimorfismos de STING son determinantes clave de la evasión inmune viral y la patogenicidad entre especies.
Estos hallazgos mejoran la comprensión de la coevolución huésped-virus y la diversidad biológica.

Palabras clave:

evasión inmune iridovirus espectro de patogenicidad polimorfismo de un solo aminoácido estimulador de genes de interferón

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