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

Eloy Cuadrado, Thijs Booiman, John L. van Hamme, Machiel H. Jansen, Karel A. van Dort, Adeline Vanderver, Gillian I. Rice, Yanick J. Crow, Neeltje A. Kootstra, Taco W. Kuijpers

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17 Citations (Scopus)


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-Goutieeres 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
Original languageEnglish
Pages (from-to)e0143613
Issue number12
Publication statusPublished - 2015

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