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ADAR1 Facilitates HIV-1 Replication in Primary CD4(+) T Cells

Unlike resting CD4(+) T cells, activated CD4(+)T cells are highly susceptible to infection of human immunodeficiency virus 1 (HIV-1). HIV-1 infects T cells and macrophages without activating the nucleic acid sensors and the anti-viral type I interferon response. Adenosine deaminase acting on RNA 1 (...

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Detalles Bibliográficos
Autores principales: Cuadrado, Eloy, Booiman, Thijs, van Hamme, John L., Jansen, Machiel H., van Dort, Karel A., Vanderver, Adeline, Rice, Gillian I., Crow, Yanick J., Kootstra, Neeltje A., Kuijpers, Taco W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4667845/
https://www.ncbi.nlm.nih.gov/pubmed/26629815
http://dx.doi.org/10.1371/journal.pone.0143613
Descripción
Sumario:Unlike resting CD4(+) T cells, activated CD4(+)T cells are highly susceptible to infection of human immunodeficiency virus 1 (HIV-1). HIV-1 infects T cells and macrophages without activating the nucleic acid sensors and the anti-viral type I interferon response. Adenosine deaminase acting on RNA 1 (ADAR1) is an RNA editing enzyme that displays antiviral activity against several RNA viruses. Mutations in ADAR1 cause the autoimmune disorder Aicardi-Goutieères syndrome (AGS). This disease is characterized by an inappropriate activation of the interferon-stimulated gene response. Here we show that HIV-1 replication, in ADAR1-deficient CD4(+)T lymphocytes from AGS patients, is blocked at the level of protein translation. Furthermore, viral protein synthesis block is accompanied by an activation of interferon-stimulated genes. RNA silencing of ADAR1 in Jurkat cells also inhibited HIV-1 protein synthesis. Our data support that HIV-1 requires ADAR1 for efficient replication in human CD4(+)T cells.