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Purification of Viral DNA for the Identification of Associated Viral and Cellular Proteins
Published on: August 31, 2017
La polimerización de actina local y el reclutamiento de dinamina en la internalización inducida por SV40 de las
Lucas Pelkmans1, Daniel Püntener, Ari Helenius
1Swiss Federal Institute of Technology Zurich (ETHZ), HPM1 Building, ETH Hönggerberg, CH-8093 Zurich, Switzerland.
Science (New York, N.Y.)
|April 20, 2002
Resumen
El virus del simio 40 (SV40) utiliza cuevas para entrar en las células, lo que desencadena reorganizaciones del citoesqueleto de actina. Este proceso, dependiente del colesterol y las tirosinacinasas, es esencial para la infección viral.
Área de la Ciencia:
- Biología celular Biología celular.
- Virología Virología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- El virus del simio 40 (SV40) es un patógeno que infecta las células del huésped.
- Los mecanismos de entrada viral son cruciales para comprender la infección y desarrollar contramedidas.
- Las caveolas son microdominios especializados de membrana involucrados en procesos celulares, incluida la endocitosis.
Objetivo del estudio:
- Para investigar el papel de las cuevas y el citoesqueleto de actina en la entrada del virus simio 40 (SV40) en las células huésped.
- Para dilucidar los mecanismos moleculares subyacentes a la endocitosis inducida por SV40.
- Para identificar los factores del huésped críticos para la infección SV40 a través de vías caveolares.
Principales métodos:
- Microscopia para observar las interacciones virus-célula huésped.
- Análisis bioquímicos para estudiar el reclutamiento de proteínas y la fosforilación.
- Inhibición genética o farmacológica de los componentes celulares clave.
Principales resultados:
- SV40 se une a las caveolas, induciendo la descomposición de la fibra de actina por estrés y el posterior reclutamiento de actina.
- Se forman parches de actina en las cuevas cargadas de virus, lo que facilita el montaje de la "cola" de actina.
- El reclutamiento de dinamina II, el colesterol y la activación de la tirosina quinasa son esenciales para la formación de vesículas e infección.
Conclusiones:
- La infección SV40 es iniciada por una endocitosis caveolar desencadenada por ligandos.
- La remodelación extensa del citoesqueleto de actina es una respuesta crítica de la célula huésped a la unión SV40.
- Las vías de señalización del colesterol y la tirosina quinasa son indispensables para la entrada infecciosa de SV40 a través de las cuevas.
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