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Transcription of interferon stimulated genes in response to Porcine rubulavirus infection in vitro
Porcine rubulavirus (PoRV) is an emerging virus causing meningo-encephalitis and reproductive failures in pigs. Little is known about the pathogenesis and immune evasion of this virus; therefore research on the mechanisms underlying tissue damage during infection is essential. To explore these mecha...
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Published in: | Brazilian journal of microbiology 2011-09, Vol.42 (3), p.1167-1175 |
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container_title | Brazilian journal of microbiology |
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creator | Flores-Ocelotl, María Del Rosario Rosas-Murrieta, Nora Hilda Vallejo-Ruiz, Verónica Reyes-Leyva, Julio Herrera-Camacho, Irma Santos-López, Gerardo |
description | Porcine rubulavirus (PoRV) is an emerging virus causing meningo-encephalitis and reproductive failures in pigs. Little is known about the pathogenesis and immune evasion of this virus; therefore research on the mechanisms underlying tissue damage during infection is essential. To explore these mechanisms, the effect of PoRV on the transcription of interferon (IFN) pathway members was analyzed in vitro by semi-quantitative RT-PCR. Ten TCID50 of PoRV stimulated transcription of IFNα, IFNβ, STAT1, STAT2, p48 and OAS genes in neuroblastoma cells, whereas infection with 100 TCID50 did not stimulate transcription levels more than non-infected cells. When the cells were primed with IFNα, infection with 1 TCDI50 of PoRV sufficed to stimulate the transcription of the same genes, but 10 and 100 TCID50 did not modify the transcription level of those genes as compared with non-infected and primed controls. MxA gene transcription was observed only when the cells were primed with IFNα and stimulated with 10 TCID50, whereas 100 TCID50 of PoRV did not modify the MxA transcription level as compared to non-infected and primed cells. Our results show that PoRV replication at low titers stimulates the expression of IFN-responsive genes in neuroblastoma cells, and suggest that replication of PoRV at higher titers inhibits the transcription of several members of the IFN pathway. These findings may contribute to the understanding of the pathogenesis of PoRV. |
doi_str_mv | 10.1590/S1517-83822011000300041 |
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Little is known about the pathogenesis and immune evasion of this virus; therefore research on the mechanisms underlying tissue damage during infection is essential. To explore these mechanisms, the effect of PoRV on the transcription of interferon (IFN) pathway members was analyzed in vitro by semi-quantitative RT-PCR. Ten TCID50 of PoRV stimulated transcription of IFNα, IFNβ, STAT1, STAT2, p48 and OAS genes in neuroblastoma cells, whereas infection with 100 TCID50 did not stimulate transcription levels more than non-infected cells. When the cells were primed with IFNα, infection with 1 TCDI50 of PoRV sufficed to stimulate the transcription of the same genes, but 10 and 100 TCID50 did not modify the transcription level of those genes as compared with non-infected and primed controls. MxA gene transcription was observed only when the cells were primed with IFNα and stimulated with 10 TCID50, whereas 100 TCID50 of PoRV did not modify the MxA transcription level as compared to non-infected and primed cells. Our results show that PoRV replication at low titers stimulates the expression of IFN-responsive genes in neuroblastoma cells, and suggest that replication of PoRV at higher titers inhibits the transcription of several members of the IFN pathway. These findings may contribute to the understanding of the pathogenesis of PoRV.</description><identifier>ISSN: 1517-8382</identifier><identifier>ISSN: 1678-4405</identifier><identifier>EISSN: 1678-4405</identifier><identifier>DOI: 10.1590/S1517-83822011000300041</identifier><identifier>PMID: 24031738</identifier><language>eng ; por</language><publisher>Brazil: Springer Nature B.V</publisher><subject>Animal diseases ; Gene expression ; Hogs ; Interferon ; MICROBIOLOGY ; Pathology</subject><ispartof>Brazilian journal of microbiology, 2011-09, Vol.42 (3), p.1167-1175</ispartof><rights>Copyright Sociedade Brasileira de Microbiologia 2011</rights><rights>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3111-cc15749f94f92591c0729d183800fba692f7142ee40e090107c82d7cbb8f8fb93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,24178,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24031738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Flores-Ocelotl, María Del Rosario</creatorcontrib><creatorcontrib>Rosas-Murrieta, Nora Hilda</creatorcontrib><creatorcontrib>Vallejo-Ruiz, Verónica</creatorcontrib><creatorcontrib>Reyes-Leyva, Julio</creatorcontrib><creatorcontrib>Herrera-Camacho, Irma</creatorcontrib><creatorcontrib>Santos-López, Gerardo</creatorcontrib><title>Transcription of interferon stimulated genes in response to Porcine rubulavirus infection in vitro</title><title>Brazilian journal of microbiology</title><addtitle>Braz J Microbiol</addtitle><description>Porcine rubulavirus (PoRV) is an emerging virus causing meningo-encephalitis and reproductive failures in pigs. Little is known about the pathogenesis and immune evasion of this virus; therefore research on the mechanisms underlying tissue damage during infection is essential. To explore these mechanisms, the effect of PoRV on the transcription of interferon (IFN) pathway members was analyzed in vitro by semi-quantitative RT-PCR. Ten TCID50 of PoRV stimulated transcription of IFNα, IFNβ, STAT1, STAT2, p48 and OAS genes in neuroblastoma cells, whereas infection with 100 TCID50 did not stimulate transcription levels more than non-infected cells. When the cells were primed with IFNα, infection with 1 TCDI50 of PoRV sufficed to stimulate the transcription of the same genes, but 10 and 100 TCID50 did not modify the transcription level of those genes as compared with non-infected and primed controls. MxA gene transcription was observed only when the cells were primed with IFNα and stimulated with 10 TCID50, whereas 100 TCID50 of PoRV did not modify the MxA transcription level as compared to non-infected and primed cells. Our results show that PoRV replication at low titers stimulates the expression of IFN-responsive genes in neuroblastoma cells, and suggest that replication of PoRV at higher titers inhibits the transcription of several members of the IFN pathway. These findings may contribute to the understanding of the pathogenesis of PoRV.</description><subject>Animal diseases</subject><subject>Gene expression</subject><subject>Hogs</subject><subject>Interferon</subject><subject>MICROBIOLOGY</subject><subject>Pathology</subject><issn>1517-8382</issn><issn>1678-4405</issn><issn>1678-4405</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp9kVtLxDAQhYMoXlb_ghZ87jqTpCZ5FPEGgoLrc2mzE8my26xJK_jvzV7UB8GHkAzznTPDCWNnCGOsDFy8YIWq1EJzDogAIPKRuMMO8VLpUkqodvP7GzpgRynNAHgFku-zAy5BoBL6kLWT2HTJRr_sfeiK4Arf9RQdxVyl3i-GedPTtHijjlLuFZHSMnSJij4UzyFa31ERhzZjHz4OK8SRXXtl-MP3MRyzPdfME51s7xF7vb2ZXN-Xj093D9dXj6UViFhai5WSxhnpDK8MWlDcTDGvD-Da5tJwp1ByIgkEBhCU1XyqbNtqp11rxIiNN77JepqHehaG2OWB9Tqs-k9YWXC-ESxjeB8o9b8S5DqPEEKrTKkNZWNIKZKrl9EvmvhZI9Srz_jH_3TrP7QLmv7ovtMXX6Cygoo</recordid><startdate>20110901</startdate><enddate>20110901</enddate><creator>Flores-Ocelotl, María Del Rosario</creator><creator>Rosas-Murrieta, Nora Hilda</creator><creator>Vallejo-Ruiz, Verónica</creator><creator>Reyes-Leyva, Julio</creator><creator>Herrera-Camacho, Irma</creator><creator>Santos-López, Gerardo</creator><general>Springer Nature B.V</general><general>Sociedade Brasileira de Microbiologia</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CLZPN</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>GPN</scope></search><sort><creationdate>20110901</creationdate><title>Transcription of interferon stimulated genes in response to Porcine rubulavirus infection in vitro</title><author>Flores-Ocelotl, María Del Rosario ; 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subjects | Animal diseases Gene expression Hogs Interferon MICROBIOLOGY Pathology |
title | Transcription of interferon stimulated genes in response to Porcine rubulavirus infection in vitro |
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