Mouse SAMHD1 Has Antiretroviral Activity and Suppresses a Spontaneous Cell-Intrinsic Antiviral Response.
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Authors
Behrendt, RaykSchumann, Tina
Gerbaulet, Alexander
Nguyen, Laura A
Schubert, Nadja
Alexopoulou, Dimitra
Berka, Ursula
Lienenklaus, Stefan
Peschke, Katrin
Gibbert, Kathrin
Wittmann, Sabine
Lindemann, Dirk
Weiss, Siegfried
Dahl, Andreas
Naumann, Ronald
Dittmer, Ulf
Kim, Baek
Mueller, Werner
Gramberg, Thomas
Roers, Axel
Issue Date
2013-08-29
Metadata
Show full item recordAbstract
Aicardi-Goutières syndrome (AGS), a hereditary autoimmune disease, clinically and biochemically overlaps with systemic lupus erythematosus (SLE) and, like SLE, is characterized by spontaneous type I interferon (IFN) production. The finding that defects of intracellular nucleases cause AGS led to the concept that intracellular accumulation of nucleic acids triggers inappropriate production of type I IFN and autoimmunity. AGS can also be caused by defects of SAMHD1, a 3' exonuclease and deoxynucleotide (dNTP) triphosphohydrolase. Human SAMHD1 is an HIV-1 restriction factor that hydrolyzes dNTPs and decreases their concentration below the levels required for retroviral reverse transcription. We show in gene-targeted mice that also mouse SAMHD1 reduces cellular dNTP concentrations and restricts retroviral replication in lymphocytes, macrophages, and dendritic cells. Importantly, the absence of SAMHD1 triggered IFN-β-dependent transcriptional upregulation of type I IFN-inducible genes in various cell types indicative of spontaneous IFN production. SAMHD1-deficient mice may be instrumental for elucidating the mechanisms that trigger pathogenic type I IFN responses in AGS and SLE.Citation
Mouse SAMHD1 Has Antiretroviral Activity and Suppresses a Spontaneous Cell-Intrinsic Antiviral Response. 2013, 4 (4):689-96 Cell RepAffiliation
Institute for Immunology, Medical Faculty Carl Gustav Carus, University of Technology Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.Journal
Cell reportsPubMed ID
23972988Type
ArticleLanguage
enISSN
2211-1247ae974a485f413a2113503eed53cd6c53
10.1016/j.celrep.2013.07.037
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