Document Detail


ADAR1 enhances HTLV-1 and HTLV-2 replication through inhibition of PKR activity.
MedLine Citation:
PMID:  25389016     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
BackgroundThe role of innate immunity in general and of type I interferon (IFN-I) in particular in HTLV-1 pathogenesis is still a matter of debate. ADAR1-p150 is an Interferon Stimulated Gene (ISG) induced by IFN-I that can edit viral RNAs. We therefore investigated whether it could play the role of an anti-HTLV factor.ResultsWe demonstrate here that ADAR1 is also expressed in the absence of IFN stimulation in activated primary T-lymphocytes that are the natural target of this virus and in HTLV-1 or HTLV-2 chronically infected T-cells. ADAR1 expression is also increased in primary lymphocytes obtained from HTLV-1 infected individuals. We show that ADAR1 enhances HTLV-1 and HTLV-2 infection in T-lymphocytes and that this proviral effect is independent from its editing activity. ADAR1 expression suppresses IFN-¿ inhibitory effect on HTLV-1 and HTLV-2 and acts through the repression of PKR phosphorylation.DiscussionThis study demonstrates that two interferon stimulated genes, i.e. PKR and ADAR1 have opposite effects on HTLV replication in vivo. The balanced expression of those proteins could determine the fate of the viral cycle in the course of infection.
Authors:
Anne Cachat; Sandrine Alais; Sébastien Chevalier; Chloé Journo; Floriane Fusil; Hélène Dutartre; Adrien Boniface; Nga Ko; Antoine Gessain; François-Loïc Cosset; Rodolphe Suspène; Jean-Pierre Vartanian; Renaud Mahieux
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-11-12
Journal Detail:
Title:  Retrovirology     Volume:  11     ISSN:  1742-4690     ISO Abbreviation:  Retrovirology     Publication Date:  2014 Nov 
Date Detail:
Created Date:  2014-11-12     Completed Date:  -     Revised Date:  2014-11-13    
Medline Journal Info:
Nlm Unique ID:  101216893     Medline TA:  Retrovirology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  93     Citation Subset:  -    
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