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CD163 en la encrucijada: un inmunomodulador explotado por virus
Jiayong Tan1, Jie Cheng1, Xiaohui Yang1
1State Key Laboratory of Swine and Poultry Breeding Industry, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou, 510642, China.
Virology journal
|January 28, 2026
Resumen
El virus de la peste porcina reproductiva y respiratoria (PRRSV) utiliza el CD163 como receptor para la entrada. La comprensión del CD163
Área de la Ciencia:
- Virología Veterinaria
- Inmunología
- Biología Molecular
Sus antecedentes:
- El virus de la peste porcina reproductiva y respiratoria (PRRSV) representa una amenaza económica significativa para la industria porcina.
- El CD163 se identifica como el principal receptor celular para la entrada del PRRSV.
- El CD163 desempeña un papel crucial en la modulación de las respuestas inmunitarias del huésped durante la infección por PRRSV.
Objetivo del estudio:
- Revisar la estructura, las funciones fisiológicas y los mecanismos del CD163 en la infección por PRRSV.
- Elucidar los roles inmunomoduladores del CD163 durante la infección por PRRSV.
- Explorar las intervenciones dirigidas al CD163 para el control del PRRSV.
Principales métodos:
- Revisión de la literatura de estudios sobre CD163 y PRRSV.
- Análisis de la expresión de CD163, el desprendimiento del ectodominio y su impacto en la polarización de los macrófagos y los perfiles de citoquinas.
- Evaluación de la manipulación del PRRSV de la señalización inflamatoria del huésped a través del CD163.
- Revisión de las estrategias terapéuticas emergentes dirigidas al CD163.
Principales resultados:
- El PRRSV explota las vías antiinflamatorias para mejorar la expresión de CD163 y facilitar la entrada del virus.
- Los estímulos proinflamatorios disminuyen la expresión de CD163, lo que restringe la replicación del PRRSV.
- El CD163 soluble (sCD163) tiene un doble papel como receptor señuelo potencial y como contribuyente a la patología inflamatoria.
- Las modificaciones dirigidas del CD163 pueden conferir resistencia al PRRSV sin comprometer las funciones esenciales del huésped.
Conclusiones:
- El CD163 es un determinante crítico de la entrada y patogénesis del PRRSV, actuando como una puerta de entrada viral y un inmunomodulador.
- El doble papel del CD163 en la infección por PRRSV ofrece nuevas dianas terapéuticas.
- El desarrollo de estrategias que bloqueen la entrada viral mientras mantienen la homeostasis inmune es clave para el control efectivo del PRRSV.
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