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 |
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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. 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.</description><identifier>ISSN: 0166-3542</identifier><identifier>EISSN: 1872-9096</identifier><identifier>DOI: 10.1016/j.antiviral.2010.05.011</identifier><identifier>PMID: 20561966</identifier><identifier>CODEN: ARSRDR</identifier><language>eng</language><publisher>Kidlington: Elsevier B.V</publisher><subject>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</subject><ispartof>Antiviral research, 2010-08, Vol.87 (2), p.249-256</ispartof><rights>2010 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright 2010 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c432t-4c14ac0a0f7e5dd175081e73a5b4278d3492dfc6fa3ad73ce40890d21a544d503</citedby><cites>FETCH-LOGICAL-c432t-4c14ac0a0f7e5dd175081e73a5b4278d3492dfc6fa3ad73ce40890d21a544d503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.antiviral.2010.05.011$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23072323$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20561966$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qian, Jun</creatorcontrib><creatorcontrib>Zhai, Aixia</creatorcontrib><creatorcontrib>Kao, Wenping</creatorcontrib><creatorcontrib>Li, Yujun</creatorcontrib><creatorcontrib>Song, Wuqi</creatorcontrib><creatorcontrib>Fu, Yingmei</creatorcontrib><creatorcontrib>Chen, Xiaobei</creatorcontrib><creatorcontrib>Zhang, Qingmeng</creatorcontrib><creatorcontrib>Wu, Jing</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Zhong, Zhaohua</creatorcontrib><creatorcontrib>Ling, Hong</creatorcontrib><creatorcontrib>Zhang, Fengmin</creatorcontrib><title>Modulation of miR-122 on persistently Borna disease virus infected human oligodendroglial cells</title><title>Antiviral research</title><addtitle>Antiviral Res</addtitle><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.</description><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>Antiviral agents</subject><subject>Biological and medical sciences</subject><subject>Borna disease virus</subject><subject>Borna disease virus - immunology</subject><subject>Borna disease virus - isolation & purification</subject><subject>Gene Expression Profiling</subject><subject>Human oligodendroglial cells</subject><subject>Humans</subject><subject>Interferon</subject><subject>Interferons - secretion</subject><subject>Medical sciences</subject><subject>microRNA-122</subject><subject>MicroRNAs - biosynthesis</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - immunology</subject><subject>Nucleic Acid Hybridization</subject><subject>Oligodendroglia - immunology</subject><subject>Oligodendroglia - virology</subject><subject>Persistent infection</subject><subject>Pharmacology. Drug treatments</subject><subject>Viral Proteins - biosynthesis</subject><issn>0166-3542</issn><issn>1872-9096</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0EotvCV4BcEKcs439xciwVUKQiJARna2pPildOvNhJpX57vNqlHHuwLI9-z_P0HmNvOWw58O7DbovzEu5DxrgVUKegt8D5M7bhvRHtAEP3nG0q2bVSK3HGzkvZAUBnhv4lOxOgOz503YbZb8mvEZeQ5iaNzRR-tFyIpr72lEsoC81LfGg-pjxj40MhLNTUvWtpwjySW8g3v9cJqzqGu-Rp9jndxYCxcRRjecVejBgLvT7dF-zX508_r67bm-9fvl5d3rROSbG0ynGFDhBGQ9p7bjT0nIxEfauE6b1Ug_Cj60aU6I10pKAfwAuOWimvQV6w98d_9zn9Waksdgrl4ABnSmuxPRiheyWeJo1UAKqeSpoj6XIqJdNo9zlMmB8sB3uowe7sYw32UIMFbWsNVfnmtGO9ncg_6v7lXoF3JwCLwzhmnF0o_zlZ7UohK3d55Khmdx8o2-ICzY58yDV861N40sxfHVuqXw</recordid><startdate>20100801</startdate><enddate>20100801</enddate><creator>Qian, Jun</creator><creator>Zhai, Aixia</creator><creator>Kao, Wenping</creator><creator>Li, Yujun</creator><creator>Song, Wuqi</creator><creator>Fu, Yingmei</creator><creator>Chen, Xiaobei</creator><creator>Zhang, Qingmeng</creator><creator>Wu, Jing</creator><creator>Li, Hui</creator><creator>Zhong, Zhaohua</creator><creator>Ling, Hong</creator><creator>Zhang, Fengmin</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>20100801</creationdate><title>Modulation of miR-122 on persistently Borna disease virus infected human oligodendroglial cells</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c432t-4c14ac0a0f7e5dd175081e73a5b4278d3492dfc6fa3ad73ce40890d21a544d503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Antibiotics. Antiinfectious agents. Antiparasitic agents</topic><topic>Antiviral agents</topic><topic>Biological and medical sciences</topic><topic>Borna disease virus</topic><topic>Borna disease virus - immunology</topic><topic>Borna disease virus - isolation & purification</topic><topic>Gene Expression Profiling</topic><topic>Human oligodendroglial cells</topic><topic>Humans</topic><topic>Interferon</topic><topic>Interferons - secretion</topic><topic>Medical sciences</topic><topic>microRNA-122</topic><topic>MicroRNAs - biosynthesis</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - immunology</topic><topic>Nucleic Acid Hybridization</topic><topic>Oligodendroglia - immunology</topic><topic>Oligodendroglia - virology</topic><topic>Persistent infection</topic><topic>Pharmacology. 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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. 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.</abstract><cop>Kidlington</cop><pub>Elsevier B.V</pub><pmid>20561966</pmid><doi>10.1016/j.antiviral.2010.05.011</doi><tpages>8</tpages></addata></record> |
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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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