Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells
Infection by porcine reproductive and respiratory syndrome virus (PRRSV) results in a weak induction of the innate immune response. There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigatio...
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| Veröffentlicht in: | Archives of virology 2004-12, Vol.149 (12), p.2453-2463 |
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| creator | Miller, L.C Laegreid, W.W Bono, J.L Chitko-McKown, C.G Fox, J.M |
| description | Infection by porcine reproductive and respiratory syndrome virus (PRRSV) results in a weak induction of the innate immune response. There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigation. To this end, we have utilized real-time PCR using SYBR Green I dye-based detection to quantify transcript abundance of the type I interferons (IFN-alpha and -beta) and IFN-beta transcriptional enhanceasome genes. In MARC-145 cells, both IFN-alpha and -beta transcript abundance were unaffected by PRRSV infection. However, stimulation of MARC-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-alpha and -beta as well as IFN-beta enhanceasome components, indicating that a type I IFN response could be induced in these cells. The double-stranded RNA induction of type I IFN transcription was significantly inhibited by dual-exposure with PRRSV. These results suggest that PRRSV infection directly interferes with type I IFN transcriptional activation early in its pathway, at the level of IFN-beta gene transcription. |
| doi_str_mv | 10.1007/s00705-004-0377-9 |
| format | Article |
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There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigation. To this end, we have utilized real-time PCR using SYBR Green I dye-based detection to quantify transcript abundance of the type I interferons (IFN-alpha and -beta) and IFN-beta transcriptional enhanceasome genes. In MARC-145 cells, both IFN-alpha and -beta transcript abundance were unaffected by PRRSV infection. However, stimulation of MARC-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-alpha and -beta as well as IFN-beta enhanceasome components, indicating that a type I IFN response could be induced in these cells. The double-stranded RNA induction of type I IFN transcription was significantly inhibited by dual-exposure with PRRSV. These results suggest that PRRSV infection directly interferes with type I IFN transcriptional activation early in its pathway, at the level of IFN-beta gene transcription.</description><identifier>ISSN: 0304-8608</identifier><identifier>EISSN: 1432-8798</identifier><identifier>DOI: 10.1007/s00705-004-0377-9</identifier><identifier>PMID: 15338318</identifier><language>eng</language><publisher>Wien: Springer</publisher><subject>Animals ; Biological and medical sciences ; Brief Report ; Cell Line ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - immunology ; Genes ; Hogs ; immune response ; Infections ; Interferon ; Interferon-alpha - biosynthesis ; Interferon-alpha - genetics ; Interferon-beta - biosynthesis ; Interferon-beta - genetics ; Microbiology ; Miscellaneous ; Porcine reproductive and respiratory syndrome virus ; Porcine respiratory and reproductive syndrome virus ; Porcine respiratory and reproductive syndrome virus - immunology ; RNA, Messenger - metabolism ; Swine ; Transcription factors ; Transcription Factors - metabolism ; Viral infections ; Virology</subject><ispartof>Archives of virology, 2004-12, Vol.149 (12), p.2453-2463</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright Springer-Verlag 2004</rights><rights>Springer-Verlag/Wien 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-936086ab7c96356bad70b63f2cab6a8a2579b37e3c13ba94a18a70b4170310be3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16319801$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15338318$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miller, L.C</creatorcontrib><creatorcontrib>Laegreid, W.W</creatorcontrib><creatorcontrib>Bono, J.L</creatorcontrib><creatorcontrib>Chitko-McKown, C.G</creatorcontrib><creatorcontrib>Fox, J.M</creatorcontrib><title>Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells</title><title>Archives of virology</title><addtitle>Arch Virol</addtitle><description>Infection by porcine reproductive and respiratory syndrome virus (PRRSV) results in a weak induction of the innate immune response. There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigation. To this end, we have utilized real-time PCR using SYBR Green I dye-based detection to quantify transcript abundance of the type I interferons (IFN-alpha and -beta) and IFN-beta transcriptional enhanceasome genes. In MARC-145 cells, both IFN-alpha and -beta transcript abundance were unaffected by PRRSV infection. However, stimulation of MARC-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-alpha and -beta as well as IFN-beta enhanceasome components, indicating that a type I IFN response could be induced in these cells. The double-stranded RNA induction of type I IFN transcription was significantly inhibited by dual-exposure with PRRSV. These results suggest that PRRSV infection directly interferes with type I IFN transcriptional activation early in its pathway, at the level of IFN-beta gene transcription.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brief Report</subject><subject>Cell Line</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - immunology</subject><subject>Genes</subject><subject>Hogs</subject><subject>immune response</subject><subject>Infections</subject><subject>Interferon</subject><subject>Interferon-alpha - biosynthesis</subject><subject>Interferon-alpha - genetics</subject><subject>Interferon-beta - biosynthesis</subject><subject>Interferon-beta - genetics</subject><subject>Microbiology</subject><subject>Miscellaneous</subject><subject>Porcine reproductive and respiratory syndrome virus</subject><subject>Porcine respiratory and reproductive syndrome virus</subject><subject>Porcine respiratory and reproductive syndrome virus - immunology</subject><subject>RNA, Messenger - metabolism</subject><subject>Swine</subject><subject>Transcription factors</subject><subject>Transcription Factors - metabolism</subject><subject>Viral infections</subject><subject>Virology</subject><issn>0304-8608</issn><issn>1432-8798</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkU-LFDEQxYMo7uzqB_CiQdBbayXp_LsIy-DqwIqg7jmk0-k1y0zSJt0D8-1NO4OrXrwkUO9Xj6p6CD0j8IYAyLelPsAbgLYBJmWjH6AVaRltlNTqIVoBq4oSoM7QeSl3ALXA-GN0RjhjihG1QmETJ58Hn1PE02H0eIOzL2OKxeMQ8ZiyC9HX2phTP7sp7D22sf8FhWynlA-4HGKf087jfchzaUIcvJt8jz9dflk3pOXY-e22PEGPBrst_unpv0A3V--_rT82158_bNaX143jIKdGszqvsJ10WjAuOttL6AQbqLOdsMpSLnXHpGeOsM7q1hJlK9ESCYxA59kFenf0Hedu53vn45Tt1ow57Gw-mGSD-VuJ4bu5TXsjQUnK22rw-mSQ04_Zl8nsQllWsNGnuRghCbRas_-CRHLGqVwcX_4D3qU5x3oFQwlluqV0gcgRcjmVkv3we2QCZonbHOM2NW6zxG107Xn-5673Had8K_DqBNji7HbINrpQ7jnBiFZAKvfiyA02GXubK3PzlVYBQAstBWc_AW0kvIM</recordid><startdate>20041201</startdate><enddate>20041201</enddate><creator>Miller, L.C</creator><creator>Laegreid, W.W</creator><creator>Bono, J.L</creator><creator>Chitko-McKown, C.G</creator><creator>Fox, J.M</creator><general>Springer</general><general>Springer Nature B.V</general><general>Springer-Verlag</general><scope>FBQ</scope><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>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20041201</creationdate><title>Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells</title><author>Miller, L.C ; Laegreid, W.W ; Bono, J.L ; Chitko-McKown, C.G ; Fox, J.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-936086ab7c96356bad70b63f2cab6a8a2579b37e3c13ba94a18a70b4170310be3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brief Report</topic><topic>Cell Line</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - immunology</topic><topic>Genes</topic><topic>Hogs</topic><topic>immune response</topic><topic>Infections</topic><topic>Interferon</topic><topic>Interferon-alpha - biosynthesis</topic><topic>Interferon-alpha - genetics</topic><topic>Interferon-beta - biosynthesis</topic><topic>Interferon-beta - genetics</topic><topic>Microbiology</topic><topic>Miscellaneous</topic><topic>Porcine reproductive and respiratory syndrome virus</topic><topic>Porcine respiratory and reproductive syndrome virus</topic><topic>Porcine respiratory and reproductive syndrome virus - immunology</topic><topic>RNA, Messenger - metabolism</topic><topic>Swine</topic><topic>Transcription factors</topic><topic>Transcription Factors - metabolism</topic><topic>Viral infections</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miller, L.C</creatorcontrib><creatorcontrib>Laegreid, W.W</creatorcontrib><creatorcontrib>Bono, J.L</creatorcontrib><creatorcontrib>Chitko-McKown, C.G</creatorcontrib><creatorcontrib>Fox, J.M</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Archives of virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miller, L.C</au><au>Laegreid, W.W</au><au>Bono, J.L</au><au>Chitko-McKown, C.G</au><au>Fox, J.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells</atitle><jtitle>Archives of virology</jtitle><addtitle>Arch Virol</addtitle><date>2004-12-01</date><risdate>2004</risdate><volume>149</volume><issue>12</issue><spage>2453</spage><epage>2463</epage><pages>2453-2463</pages><issn>0304-8608</issn><eissn>1432-8798</eissn><abstract>Infection by porcine reproductive and respiratory syndrome virus (PRRSV) results in a weak induction of the innate immune response. There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigation. To this end, we have utilized real-time PCR using SYBR Green I dye-based detection to quantify transcript abundance of the type I interferons (IFN-alpha and -beta) and IFN-beta transcriptional enhanceasome genes. In MARC-145 cells, both IFN-alpha and -beta transcript abundance were unaffected by PRRSV infection. However, stimulation of MARC-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-alpha and -beta as well as IFN-beta enhanceasome components, indicating that a type I IFN response could be induced in these cells. The double-stranded RNA induction of type I IFN transcription was significantly inhibited by dual-exposure with PRRSV. These results suggest that PRRSV infection directly interferes with type I IFN transcriptional activation early in its pathway, at the level of IFN-beta gene transcription.</abstract><cop>Wien</cop><cop>New York, NY</cop><pub>Springer</pub><pmid>15338318</pmid><doi>10.1007/s00705-004-0377-9</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Brief Report Cell Line Fundamental and applied biological sciences. Psychology Gene Expression Regulation - immunology Genes Hogs immune response Infections Interferon Interferon-alpha - biosynthesis Interferon-alpha - genetics Interferon-beta - biosynthesis Interferon-beta - genetics Microbiology Miscellaneous Porcine reproductive and respiratory syndrome virus Porcine respiratory and reproductive syndrome virus Porcine respiratory and reproductive syndrome virus - immunology RNA, Messenger - metabolism Swine Transcription factors Transcription Factors - metabolism Viral infections Virology |
| title | Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells |
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