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La retrotransposición de la ciclofilina A en TRIM5 explica la resistencia del mono búho al VIH-1

David M Sayah¹, Elena Sokolskaja, Lionel Berthoux

¹Department of Microbiology, Columbia University, College of Physicians and Surgeons, 701 West 168th Street, HHSC 1502 New York, New York 10032, USA.

|July 10, 2004

Resumen

Los monos búho restringen el virus de la inmunodeficiencia humana tipo 1 (VIH-1) a través de TRIMCyp, una proteína de fusión. Este gen antiviral TRIMCyp surgió de un retrotransposón LINE-1 que inserta el ADN de la ciclofilina A (CypA) en el gen TRIM5.

Área de la Ciencia:

Virología Virología.
Genética La genética.
Biología evolutiva Biología evolutiva.

Sus antecedentes:

Los primates del Viejo Mundo poseen TRIM5-alfa, que inhibe el virus de la inmunodeficiencia humana tipo 1 (VIH-1) después de la entrada.
La ciclofilina A (CypA) que se une a la cápside viral normalmente protege al VIH-1 de la restricción en las células humanas.
Los monos búho son únicos entre los primates del Nuevo Mundo por exhibir restricción posterior a la entrada del VIH-1.

Objetivo del estudio:

Investigar el mecanismo detrás de la restricción posterior a la entrada del VIH-1 en el mono búho.
Para identificar los factores genéticos específicos responsables de esta actividad antiviral.
Para entender el origen evolutivo de esta defensa específica de los primates.

Principales métodos:

La interferencia de ARN (RNAi) se utilizó para derribar la ciclofilina A (CypA) del mono búho.
Se realizó la reintroducción de la proteína CypA en las células tratadas.
La detección de objetivos adicionales de RNAi identificó TRIMCyp.
Los experimentos de transferencia de genes se llevaron a cabo utilizando células humanas y de rata.

Principales resultados:

La eliminación del CypA del mono búho se correlacionó con una reducción de la actividad anti-VIH-1, pero la reintroducción no la restauró.
TRIMCyp, una proteína de fusión TRIM5-CypA, fue identificada como el factor responsable de la restricción posterior a la entrada.
TRIMCyp confirió restricción del VIH-1 cuando se transfirió a células humanas y ratas.
El gen TRIMCyp probablemente se originó a partir de una inserción mediada por retrotransposón LINE-1 de ADNc de CypA en el locus TRIM5.

Conclusiones:

TRIMCyp es el mediador clave de la restricción post-entrada del VIH-1 en los monos búho.
Este gen quimérico representa un nuevo mecanismo evolutivo, con un retrotransposón que facilita el baraje de exones en los vertebrados.
La capacidad de TRIMCyp para bloquear la infección por VIH-1 en diferentes especies destaca su potente función antiviral.

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