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Vif secuestra CBF-β para degradar APOBEC3G y promover la infección por el VIH-1
Stefanie Jäger1, Dong Young Kim, Judd F Hultquist
1Department of Cellular and Molecular Pharmacology, University of California-San Francisco, San Francisco, California 94158, USA.
Nature
|December 23, 2011
Resumen
La proteína Vif del virus de la inmunodeficiencia humana tipo 1 (VIH-1) secuestra la maquinaria celular para degradar APOBEC3G, un factor antiviral clave. Este estudio revela que el cofactor de transcripción CBF-β es esencial para este proceso, ofreciendo un potencial objetivo terapéutico.
Área de la Ciencia:
- Virología Virología.
- Biología Molecular Biología Molecular
- Inmunología Inmunología.
Sus antecedentes:
- Los factores de restricción celular como APOBEC3G inhiben la replicación viral.
- La proteína Vif del virus de la inmunodeficiencia humana tipo 1 (VIH-1) contrarresta esta defensa al dirigirse a APOBEC3G para su degradación.
- El complejo de ubiquitina ligasa secuestrado por Vif incluye CUL5, ELOC, ELOB y una proteína RING-box.
Objetivo del estudio:
- Para identificar factores de huésped adicionales reclutados por el VIH-1 Vif al complejo de ubiquitina ligasa.
- Para aclarar el papel de estos factores en la degradación de APOBEC3G y la infectividad viral.
- Investigar la conservación de este mecanismo en el Virus de Inmunodeficiencia Simio (SIV).
Principales métodos:
- Etiqueta de afinidad / espectrometría de masas de purificación para identificar las proteínas que interactúan con Vif.
- Reconstitución de un ensamblaje recombinante de seis proteínas para ensayos de actividad in vitro.
- RNA knockdown y estudios de complementación genética para evaluar la función de las proteínas in vivo.
- Investigación de la interacción de SIV Vif con APOBEC3G y CBF-β.
Principales resultados:
- El VIH-1 Vif recluta el cofactor de transcripción CBF-β al complejo de ubiquitina ligasa basado en CUL5.
- El CBF-β es necesario para la poliubiquitinación y degradación específica de APOBEC3G por el complejo Vif-ligasa.
- El CBF-β es esencial para la infectividad del VIH-1 al permitir la degradación de APOBEC3G mediada por Vif.
- SIV Vif también utiliza CBF-β para degradar el APOBEC3G del macaco rhesus, lo que demuestra la conservación funcional.
Conclusiones:
- El CBF-β es un cofactor huésped crítico para la degradación APOBEC3G mediada por el VIH-1 Vif.
- La interrupción de la interacción CBF-β-Vif representa una estrategia terapéutica potencial contra el VIH-1.
- Los hallazgos destacan un mecanismo conservado de evasión viral en los lentivirus de primates.
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