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La entrada del VIH-1 en las células CD4+ está mediada por el receptor de quimioquinas CC-CKR-5
T Dragic1, V Litwin, G P Allaway
1The Aaron Diamond AIDS Research Center, The Rockefeller University, New York 10016, USA.
Nature
|June 20, 1996
Resumen
Las beta-quimiocinas como MIP-1alfa, MIP-1beta y RANTES inhiben la entrada del VIH-1 en las células T CD4+. El receptor CC-quimioquinreceptor 5 (CC-CKR-5) ha sido identificado como un factor clave para la infección por NSI VIH-1.
Área de la Ciencia:
- Inmunología Inmunología.
- Virología Virología.
- Biología celular Biología celular.
Sus antecedentes:
- Se sabe que las beta-quimiocinas (MIP-1alfa, MIP-1beta, RANTES) inhiben la infección por ciertas cepas del virus de la inmunodeficiencia humana tipo 1 (VIH-1).
- Las células T CD4 + de algunos individuos no infectados expuestos al VIH-1 exhiben resistencia a la infección por NSI VIH-1 y producen beta-quimiocinas elevadas.
Objetivo del estudio:
- Investigar el mecanismo por el cual las beta-quimiocinas inhiben la infección por el VIH-1.
- Para identificar el receptor celular involucrado en la entrada y fusión del NSI VIH-1.
Principales métodos:
- Prueba para medir la inhibición del VIH-1 por las beta-quimiocinas.
- Pruebas de fusión celular para evaluar la fusión de membranas mediada por el medio ambiente.
- Análisis de la expresión de los receptores beta-quimioquinas en las células CD4+.
Principales resultados:
- MIP-1alpha, MIP-1beta y RANTES inhiben la infección por NSI VIH-1 en la etapa de entrada.
- Estas quimiocinas también bloquean la fusión de membrana celular-célula mediada por el entorno.
- La expresión del receptor 5 de la quimioquina CC (CC-CKR-5) en las células CD4+ confiere susceptibilidad a la infección por NSI VIH-1 y a la fusión mediada por el entorno.
- CC-CKR-5 se identifica como un segundo receptor para las cepas primarias de NSI del VIH-1.
Conclusiones:
- Las beta-quimiocinas juegan un papel crucial en la restricción de la infección por NSI VIH-1.
- CC-CKR-5 es un receptor celular crítico que media la entrada y la fusión del NSI VIH-1, actuando como un co-receptor para el virus.
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