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La teterina inhibe la liberación de retrovirus y es antagonizada por el Vpu del VIH-1
Stuart J D Neil1, Trinity Zang, Paul D Bieniasz
1Aaron Diamond AIDS Research Center and Laboratory of Retrovirology, The Rockefeller University, 455 First Avenue, New York, New York 10016, USA.
Nature
|January 18, 2008
Resumen
Las células humanas tienen una defensa antiviral llamada tetherinas que atrapan las partículas de virus. Los investigadores identificaron el CD317 como una teterina, crucial para inhibir la liberación de retrovirus y un objetivo para las terapias contra el VIH / SIDA.
Área de la Ciencia:
- Virología Virología.
- Inmunología Inmunología.
- Biología celular Biología celular.
Sus antecedentes:
- Las células humanas poseen mecanismos antivirales intrínsecos que restringen la liberación de retrovirus y partículas de virus envueltas.
- Esta actividad antiviral está mediada por los tethers de proteínas, llamados tetherins, que retienen los viriones en las superficies celulares infectadas.
- La proteína accesoria Vpu del VIH-1 antagoniza esta actividad antiviral mediada por la teterina.
Objetivo del estudio:
- Para identificar la naturaleza molecular de la tetherin celular.
- Para dilucidar la relación funcional entre CD317, Vpu y liberación de partículas retrovirales.
- Explorar el potencial terapéutico de dirigirse a las interacciones de Vpu-teterina en el VIH/SIDA.
Principales métodos:
- Se emplearon restricciones deductivas y análisis de la expresión génica para identificar la tetherin.
- Los niveles de expresión de CD317 se correlacionaron con la dependencia de Vpu para la liberación viral.
- Se realizaron estudios de agotamiento de CD317 y co-localización de Vpu.
Principales resultados:
- CD317 fue identificado como una tetherin, una proteína de membrana de función desconocida.
- La expresión de CD317 se correlacionó con e indujo un requerimiento de Vpu en la liberación del virus del VIH-1 y la leucemia murina.
- El agotamiento de CD317 abolió el requisito de Vpu para la liberación del VIH-1, lo que demuestra el papel de CD317 en la retención de viriones.
- La retención de virión mediada por CD317 en las superficies celulares y dentro de los compartimentos endocíticos, un efecto inhibido por Vpu.
Conclusiones:
- CD317 funciona como una teterina, restringiendo la liberación del virus envuelto.
- Vpu antagoniza la actividad antiviral de CD317 al interrumpir la retención de viriones.
- Dirigirse a la función Vpu para movilizar la actividad antiviral de la tetherina presenta una potencial estrategia terapéutica para el VIH/SIDA.
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