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Updated: Feb 4, 2026
11:28
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
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Contrarrestar los factores de transcripción FOX regula epigenéticamente el equilibrio lítico-latente del herpesvirus
Yuhang Xiang1,2,3, Xiyuan Yang1,2,3, Juncheng Zhang1,2,3
1State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Nature communications
|February 2, 2026
Resumen
Los factores de transcripción del huésped, las proteínas forkhead box (FOX), controlan la latencia del virus del herpes simple (HSV). Su equilibrio dicta la persistencia viral y la reactivación, ofreciendo nuevas dianas terapéuticas para curar las infecciones por HSV.
Área de la Ciencia:
- Virología
- Biología Molecular
- Epigenética
Sus antecedentes:
- La persistencia del virus del herpes simple (VSH) a través del equilibrio lítico-latente dificulta la curación de la enfermedad.
- La latencia del VSH se establece en las neuronas después de la infección lítica y se reactiva por el estrés.
- Los mecanismos que rigen el equilibrio lítico-latente del VSH son poco conocidos.
Objetivo del estudio:
- Identificar los factores de transcripción del huésped que regulan la replicación y latencia del VSH.
- Investigar el papel de las proteínas forkhead box (FOX) en el equilibrio lítico-latente del VSH-1.
- Elucidar los mecanismos epigenéticos subyacentes a la regulación génica viral mediada por proteínas FOX.
Principales métodos:
- Se evaluó la actividad de los factores de transcripción FOX en el VSH-1 y otros alfaherpesvirus.
- Se comparó la expresión de genes FOX en células neuronales frente a células no neuronales.
- Se utilizaron estrategias de knockdown y sobreexpresión en cultivos neuronales y modelos in vivo.
- Se investigaron las interacciones de las proteínas FOX con genomas virales y cofactores epigenéticos.
Principales resultados:
- Los factores de transcripción FOX regulan diferencialmente la replicación del VSH.
- Las neuronas expresan preferentemente genes FOXK represivos, mientras que las células no neuronales/estresadas expresan genes FOX activadores.
- La reducción de Foxk1 o la sobreexpresión de genes FOX activadores indujeron la reactivación del VSH a partir de la latencia.
- Las proteínas FOX se unen al genoma viral de forma no específica y reclutan modificadores epigenéticos (CBP/P300, SIN3A/MAX).
Conclusiones:
- El equilibrio lítico-latente viral se rige por la abundancia relativa de factores de transcripción FOX contrapuestos.
- Las proteínas FOX modulan la accesibilidad de la cromatina viral a través del reclutamiento de cofactores epigenéticos.
- La targeting de las proteínas FOX y su maquinaria epigenética asociada presenta una estrategia novedosa para controlar la persistencia del VSH.
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