Open AccessADAR1 Facilitates HIV-1 Replication in Primary CD4+ T Cells
Author(s) -
Eloy Cuadrado,
Thijs Booiman,
John L. van Hamme,
Machiel H. Jansen,
Karel A. van Dort,
Adeline Vanderver,
Gillian Rice,
Yanick J. Crow,
Neeltje A. Kootstra,
Taco W. Kuijpers
Publication year - 2015
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0143613
Subject(s) - jurkat cells , viral replication , biology , rna , virology , interferon , gene silencing , adenosine deaminase , rna silencing , gene , rna interference , microbiology and biotechnology , t cell , virus , adenosine , immune system , immunology , genetics , biochemistry
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.