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Uso del receptor del enterovirus D68: desde la unión estática hasta la entrada dinámica

Dongxue Liu1,2, Zhilin Ji3, Xiangyu Zheng4,5

  • 1Institute of Virology and AIDS Research, The First Hospital of Jilin University, Changchun, Jilin, China.

Journal of virology
|December 30, 2025
PubMed
Resumen

El enterovirus D68 (EV-D68) utiliza múltiples receptores, incluida la sialic acid, ICAM-5 y MFSD6, para infectar células. Esta plasticidad del receptor explica su propagación en los sistemas respiratorio y nervioso, guiando el desarrollo de nuevas terapias.

Palabras clave:
ICAM-5MFSD6mielitis flácida agudaenterovirus D68sialic acidentrada viralreceptor viral

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Área de la Ciencia:

  • Virología; Biología Molecular; Inmunología

Sus antecedentes:

  • El enterovirus D68 (EV-D68) es un patógeno reemergente que causa enfermedad respiratoria grave y mielitis flácida aguda (AFM).
  • Los mecanismos de entrada viral son clave para comprender el tropismo y la patogénesis del EV-D68.
  • Los modelos anteriores se centraron en el ácido siálico, pero los descubrimientos recientes revelan un panorama de receptores más complejo.

Objetivo del estudio:

  • Revisar la comprensión evolutiva del uso de receptores de EV-D68.
  • Sintetizar el conocimiento actual sobre los factores de unión viral y los receptores de entrada.
  • Explorar las implicaciones de la versatilidad de los receptores para la evolución viral y las estrategias terapéuticas.

Principales métodos:

  • Revisión de la literatura de estudios sobre las interacciones de los receptores de EV-D68.
  • Análisis de receptores virales establecidos y recién identificados.
  • Discusión de la importancia funcional del uso de receptores en diferentes tipos de células.

Principales resultados:

  • El ácido siálico actúa como factor de unión y desencadenante de la desunión para las cepas más antiguas de EV-D68.
  • ICAM-5 es un receptor específico de neuronas que explica el neurotropismo en la AFM.
  • MFSD6 se identifica como un receptor de entrada crucial para diversas cepas de EV-D68 en células respiratorias y neuronales.

Conclusiones:

  • EV-D68 exhibe una notable plasticidad de receptores, utilizando ácido siálico, ICAM-5 y MFSD6.
  • Esta adaptabilidad influye en el tropismo tisular, la evolución viral y la manifestación de la enfermedad.
  • La comprensión de las interacciones receptor-virus, especialmente la interfaz MFSD6, es crucial para el desarrollo de nuevas terapias contra el EV-D68.