Modulation of miR-122 on persistently Borna disease virus infected human oligodendroglial cells

Using RNAhybrid software we found the predicted binding of complementary sequences between miR-122 and viral mRNAs, may be important for the antiviral effect of miR-122 on Borna disease virus (BDV). A moderate expression of miR-122 was identified in human oligodendroglial cells (OL), but with a much...

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Veröffentlicht in:Antiviral research 2010-08, Vol.87 (2), p.249-256
Hauptverfasser: Qian, Jun, Zhai, Aixia, Kao, Wenping, Li, Yujun, Song, Wuqi, Fu, Yingmei, Chen, Xiaobei, Zhang, Qingmeng, Wu, Jing, Li, Hui, Zhong, Zhaohua, Ling, Hong, Zhang, Fengmin
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container_end_page 256
container_issue 2
container_start_page 249
container_title Antiviral research
container_volume 87
creator Qian, Jun
Zhai, Aixia
Kao, Wenping
Li, Yujun
Song, Wuqi
Fu, Yingmei
Chen, Xiaobei
Zhang, Qingmeng
Wu, Jing
Li, Hui
Zhong, Zhaohua
Ling, Hong
Zhang, Fengmin
description Using RNAhybrid software we found the predicted binding of complementary sequences between miR-122 and viral mRNAs, may be important for the antiviral effect of miR-122 on Borna disease virus (BDV). A moderate expression of miR-122 was identified in human oligodendroglial cells (OL), but with a much lower level of miR-122 in BDV persistent infection (OL/BDV) and cells transfected with BDV gene expression vectors. Over-expression of miR-122 and specific blocking experiments demonstrated that miR-122 was able to specifically inhibit BDV protein synthesis, viral gene replication and transcription, and induce the secretion/synthesis of interferon (IFN) in OL and OL/BDV cells. The abolishment of miR-122 by AMO-122 inhibited endogenous IFN induction by IFN-beta. These results indicate that miR-122 can exert direct antiviral function by inhibiting BDV translation and replication on one hand, while acting indirectly through IFN to increase the host innate immunity to modulate the virus–host interactions on the other hand.
doi_str_mv 10.1016/j.antiviral.2010.05.011
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A moderate expression of miR-122 was identified in human oligodendroglial cells (OL), but with a much lower level of miR-122 in BDV persistent infection (OL/BDV) and cells transfected with BDV gene expression vectors. Over-expression of miR-122 and specific blocking experiments demonstrated that miR-122 was able to specifically inhibit BDV protein synthesis, viral gene replication and transcription, and induce the secretion/synthesis of interferon (IFN) in OL and OL/BDV cells. The abolishment of miR-122 by AMO-122 inhibited endogenous IFN induction by IFN-beta. 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subjects Antibiotics. Antiinfectious agents. Antiparasitic agents
Antiviral agents
Biological and medical sciences
Borna disease virus
Borna disease virus - immunology
Borna disease virus - isolation & purification
Gene Expression Profiling
Human oligodendroglial cells
Humans
Interferon
Interferons - secretion
Medical sciences
microRNA-122
MicroRNAs - biosynthesis
MicroRNAs - genetics
MicroRNAs - immunology
Nucleic Acid Hybridization
Oligodendroglia - immunology
Oligodendroglia - virology
Persistent infection
Pharmacology. Drug treatments
Viral Proteins - biosynthesis
title Modulation of miR-122 on persistently Borna disease virus infected human oligodendroglial cells
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