Induction of stress granules by interferon and down-regulation by the cellular RNA adenosine deaminase ADAR1

Abstract Measles virus (MV) deficient in C protein ( Cko ) expression efficiently induces both stress granules (SG) and interferon (IFNβ), whereas isogenic wild-type (WT) and V mutant ( Vko ) viruses do not. We therefore examined the effect of IFNβ pretreatment on SG formation, and the roles played...

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Bibliographic Details
Published in:Virology (New York, N.Y.) N.Y.), 2014-04, Vol.454, p.299-310
Main Authors: John, Lijo, Samuel, Charles E
Format: Article
Language:English
Subjects:
Adenosine Deaminase - immunology
Adenosine Deaminase - metabolism
Adenosine deaminase acting on RNA (ADAR)
Animals
Cercopithecus aethiops
HeLa Cells
Humans
Infectious Disease
Interferon (IFN)
Interferon-beta - immunology
Interferon-beta - metabolism
Measles virus
Morbillivirus - genetics
Morbillivirus - immunology
Protein Biosynthesis
RNA-Binding Proteins
Signal transducers and activators of transcription (STAT)
Stress granules (SG)
Vero Cells
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Summary:Abstract Measles virus (MV) deficient in C protein ( Cko ) expression efficiently induces both stress granules (SG) and interferon (IFNβ), whereas isogenic wild-type (WT) and V mutant ( Vko ) viruses do not. We therefore examined the effect of IFNβ pretreatment on SG formation, and the roles played by the IFN-inducible double-stranded (ds) RNA-dependent protein kinase (PKR) and dsRNA adenosine deaminase (ADAR1). SG formation in ADAR1-sufficient cells infected with WT or Vko mutant virus was enhanced by IFN treatment and was PKR-dependent. SG formation in Cko virus-infected cells was already high without IFN treatment and was not further enhanced by IFN. IFN treatment alone, in the absence of infection, induced SG formation in ADAR1-deficient but not ADAR1-sufficient cells. Type I IFN-induced enhancement in SG formation occurred by a canonical IFN signaling response dependent upon STAT1 and STAT2. These results further establish ADAR1 as a suppressor of the interferon and SG innate immune responses.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2014.02.025