The Tat Inhibitor Didehydro-Cortistatin A Prevents HIV-1 Reactivation from Latency
ABSTRACT Antiretroviral therapy (ART) inhibits HIV-1 replication, but the virus persists in latently infected resting memory CD4+ T cells susceptible to viral reactivation. The virus-encoded early gene product Tat activates transcription of the viral genome and promotes exponential viral production....
Guardado en:
Autores principales: | Guillaume Mousseau, Cari F. Kessing, Rémi Fromentin, Lydie Trautmann, Nicolas Chomont, Susana T. Valente |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
American Society for Microbiology
2015
|
Materias: | |
Acceso en línea: | https://doaj.org/article/6842f7e80f224a9ebc119c819dd92917 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
Ejemplares similares
-
Resistance to the Tat Inhibitor Didehydro-Cortistatin A Is Mediated by Heightened Basal HIV-1 Transcription
por: Guillaume Mousseau, et al.
Publicado: (2019) -
Unexpected Mutations in HIV-1 That Confer Resistance to the Tat Inhibitor Didehydro-Cortistatin A
por: Andrew P. Rice
Publicado: (2019) -
Didehydro-Cortistatin A Inhibits HIV-1 by Specifically Binding to the Unstructured Basic Region of Tat
por: Sonia Mediouni, et al.
Publicado: (2019) -
Splicing Factor 3B Subunit 1 Interacts with HIV Tat and Plays a Role in Viral Transcription and Reactivation from Latency
por: George B. Kyei, et al.
Publicado: (2018) -
Long noncoding RNA NRON contributes to HIV-1 latency by specifically inducing tat protein degradation
por: Jun Li, et al.
Publicado: (2016)