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Un modelo atómico de la cápside-SP1 del VIH revela estructuras que regulan el ensamblaje y la maduración

Florian K M Schur¹, Martin Obr², Wim J H Hagen³

¹Structural and Computational Biology Unit, European Molecular Biology Laboratory, Meyerhofstraße 1, 69117 Heidelberg, Germany. Molecular Medicine Partnership Unit, European Molecular Biology Laboratory-Universitätsklinikum Heidelberg, Heidelberg, Germany.

Science (New York, N.Y.)

|July 16, 2016

Resumen

Los inhibidores de la maduración bloquean la infectividad del VIH-1 estabilizando las estructuras virales inmaduras, impidiendo la escisión de la poliproteína Gag esencial. Este estudio revela la estructura atómica del VIH-1 inmaduro, detallando las interacciones a las que se dirigen las IMS.

Área de la Ciencia:

Virología
Biología estructural
La bioquímica

Sus antecedentes:

El virus de inmunodeficiencia humana inmaduro tipo 1 (VIH-1) se ensambla y brota de la membrana celular.
La escisión proteolítica de la poliproteína Gag desencadena la maduración estructural, lo que hace que el virus sea infeccioso.
Los inhibidores de la maduración (IM) bloquean este proceso, eliminando la infectividad al dirigirse a la región CA (cápsida) y SP1 (péptido espaciador 1) de Gag.

Objetivo del estudio:

Determinar la estructura de alta resolución de la región CA-SP1 dentro de las partículas inmaduras del VIH-1.
Para aclarar las interacciones moleculares que rigen el ensamblaje y la maduración del VIH-1.
Comprender el mecanismo de acción de los inhibidores de la maduración (IM).

Principales métodos:

Tomografía criolectrónica optimizada (CT criogénica).
El subtomograma promedio para lograr una resolución de 3,9 angstroms.
Construcción del modelo atómico de la región CA-SP1.

Principales resultados:

Se resolvió la estructura de la región CA-SP1 en partículas de VIH-1 inmaduras ensambladas a una resolución de 3,9 angstroms.
Reveló una red detallada de interacciones intra e intermoleculares esenciales para el ensamblaje inmaduro del VIH-1.
Se demostró que el sitio de escisión de CA-SP1 es inaccesible para la proteasa en estado inmaduro.

Conclusiones:

Es probable que los inhibidores de la maduración eviten la escisión de CA-SP1 al estabilizar la estructura viral inmadura.
Los conocimientos estructurales proporcionan una base para la comprensión de la resistencia al IM, que puede surgir de la desestabilización de estas interacciones.

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