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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
La pérdida de secuencias de ADN viral integradas en células poliomatransformadas está asociada con una función viral
Cell
|July 1, 1979
Resumen
El ADN del virus del polioma se puede perder de las células de rata transformadas, devolviéndolas a un estado normal. Esta pérdida de ADN, que implica la escisión, requiere la función viral A (antigeno T grande) para la replicación espontánea del ADN viral.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Virología Virología.
- Biología celular Biología celular.
Sus antecedentes:
- Las células de rata transformadas por el virus del polioma albergan ADN viral integrado y no integrado.
- El ADN viral no integrado surge de la replicación espontánea del ADN viral integrado, controlado por el locus A viral.
Objetivo del estudio:
- Para investigar si la inducción de la replicación del ADN viral conduce a la pérdida de ADN viral integrado, similar a la curación lisogénica bacteriana.
- Para determinar si la función viral A es esencial para este proceso de "curación".
Principales métodos:
- Selección y análisis de células revertentes de poblaciones de ratas transformadas por el virus del polioma.
- Pruebas de inmunofluorescencia para el antígeno T del polioma y experimentos de rescate de virus.
- Análisis de enzimas de restricción de secuencias de ADN viral integradas en líneas celulares parentales y curadas.
- Comparación de las frecuencias de "curado" en células transformadas por el virus del polioma tipo salvaje y mutante ts-a a diferentes temperaturas.
Principales resultados:
- Una proporción significativa de los revertentes perdió el antígeno polioma T y la capacidad de rescate viral, lo que indica la pérdida de ADN viral integrado.
- Las líneas parentales mostraron repeticiones en tándem de ADN viral integrado, que generalmente estaban ausentes en los derivados curados.
- Las células transformadas por el mutante ts-a exhibieron frecuencias de "curado" más altas a la temperatura permisiva (33°C) que a la temperatura no permisiva (39°C).
Conclusiones:
- La pérdida del ADN viral del polioma integrado ocurre a una tasa alta en las células transformadas de ratas, lo que lleva a una reversión parcial o completa a un fenotipo normal.
- Esta pérdida implica un evento de escisión y depende de la función del polioma A (antígeno T grande).
- La asociación ADN viral-ADN huésped es altamente estable en ausencia de un producto genético A funcional.
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