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El VIH-1 Nef promueve la infección al excluir SERINC5 de la incorporación de viriones
Annachiara Rosa1, Ajit Chande1, Serena Ziglio1
1University of Trento, Centre for Integrative Biology, 38123 Trento, Italy.
Nature
|September 30, 2015
Resumen
La proteína Nef del virus de la inmunodeficiencia humana tipo 1 (VIH-1) contrarresta la actividad antiviral de SERINC5, una proteína huésped que inhibe la infectividad del VIH-1. Nef previene la incorporación de SERINC5 en nuevas partículas virales, aumentando así la propagación del virus.
Área de la Ciencia:
- Virología
- Biología celular
- Inmunología
Sus antecedentes:
- La proteína Nef del VIH-1 modula los procesos de las células huésped, aumentando la infectividad viral a través de mecanismos desconocidos.
- Los factores del huésped que influyen en la replicación y propagación del VIH-1 son objetivos críticos para la intervención terapéutica.
Objetivo del estudio:
- Identificar los factores del huésped que regulan la infectividad de los viriones del VIH-1.
- Esclarecer el mecanismo por el cual el VIH-1 Nef aumenta la infectividad viral.
Principales métodos:
- Pruebas de co-inmunoprecipitación e inmunofluorescencia para identificar las interacciones de las proteínas del huésped con Nef.
- Análisis de la composición de las partículas virales y la infectividad en presencia o ausencia de proteínas SERINC.
- Microscopia confocal para rastrear la localización de SERINC5 en las células huésped durante el brote del VIH-1.
Principales resultados:
- SERINC5 y SERINC3 fueron identificados como potentes inhibidores de la infectividad de las partículas del VIH-1.
- SERINC5 se localiza en la membrana plasmática y se incorpora a los viriones en ciernes, reduciendo la infectividad.
- El VIH-1 Nef contrarresta el SERINC5 redirigiéndolo a los endosomas Rab7-positivos, excluyéndolo de los viriones.
- La capacidad de Nef para contrarrestar SERINC5 se conserva en los lentivirus de primates y converge con el virus de la leucemia murina glicosilado Gag.
Conclusiones:
- SERINC5 es un factor crítico de restricción del huésped que inhibe la infectividad del VIH-1.
- El VIH-1 Nef ha evolucionado para antagonizar SERINC5, lo que representa un paso clave en la patogénesis viral.
- La potente actividad antirretroviral de SERINC5 destaca su potencial como objetivo terapéutico.
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