Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway
The induction of an antiviral state by type I interferons (IFN) was evaluated in primary trigeminal ganglion cell cultures using herpes simplex virus type 1 (HSV-1). Cells treated with mouse IFN-β consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-...
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| Veröffentlicht in: | Journal of neuroimmunology 2003-08, Vol.141 (1), p.40-46 |
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| creator | Carr, Daniel J.J. Al-khatib, Khaldun James, Cassandra M. Silverman, Robert |
| description | The induction of an antiviral state by type I interferons (IFN) was evaluated in primary trigeminal ganglion cell cultures using herpes simplex virus type 1 (HSV-1). Cells treated with mouse IFN-β consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-α1, IFN-α4, IFN-α5, IFN-α6, or IFN-α9. The antiviral efficacy was dose-dependent and correlated with the induction of the IFN-inducible, antiviral genes, 2′–5′ oligoadenylate synthetase (OAS) and double-stranded RNA-dependent protein kinase. In trigeminal ganglion cells deficient in the downstream effector molecule of the OAS pathway, RNase L, the antiviral state induced by IFN-β was lost. |
| doi_str_mv | 10.1016/S0165-5728(03)00216-9 |
| format | Article |
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Cells treated with mouse IFN-β consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-α1, IFN-α4, IFN-α5, IFN-α6, or IFN-α9. The antiviral efficacy was dose-dependent and correlated with the induction of the IFN-inducible, antiviral genes, 2′–5′ oligoadenylate synthetase (OAS) and double-stranded RNA-dependent protein kinase. In trigeminal ganglion cells deficient in the downstream effector molecule of the OAS pathway, RNase L, the antiviral state induced by IFN-β was lost.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/S0165-5728(03)00216-9</identifier><identifier>PMID: 12965252</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Antiviral Agents - deficiency ; Antiviral Agents - genetics ; Antiviral Agents - physiology ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Endoribonucleases - deficiency ; Endoribonucleases - genetics ; Endoribonucleases - physiology ; Female ; Gene Expression Regulation, Viral - immunology ; Herpes simplex virus ; Herpes simplex virus 1 ; Herpesvirus 1, Human - genetics ; Herpesvirus 1, Human - immunology ; HSV-1 ; IFN-α ; IFN-β ; Immunity, Innate - genetics ; Immunophenotyping ; Interferon-beta - physiology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Neuroimmunology ; OAS ; PKR ; Signal Transduction - genetics ; Signal Transduction - immunology ; Transfection ; Trigeminal Ganglion - cytology ; Trigeminal Ganglion - enzymology ; Trigeminal Ganglion - immunology ; Trigeminal Ganglion - virology ; Vero Cells ; Virus Replication - genetics ; Virus Replication - immunology</subject><ispartof>Journal of neuroimmunology, 2003-08, Vol.141 (1), p.40-46</ispartof><rights>2003 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-1fda7ece30c5d7701aff62c0c8dfb40eedfdea81c8609d2b2f0323c6713307c63</citedby><cites>FETCH-LOGICAL-c494t-1fda7ece30c5d7701aff62c0c8dfb40eedfdea81c8609d2b2f0323c6713307c63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0165-5728(03)00216-9$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,778,782,883,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12965252$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Carr, Daniel J.J.</creatorcontrib><creatorcontrib>Al-khatib, Khaldun</creatorcontrib><creatorcontrib>James, Cassandra M.</creatorcontrib><creatorcontrib>Silverman, Robert</creatorcontrib><title>Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>The induction of an antiviral state by type I interferons (IFN) was evaluated in primary trigeminal ganglion cell cultures using herpes simplex virus type 1 (HSV-1). Cells treated with mouse IFN-β consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-α1, IFN-α4, IFN-α5, IFN-α6, or IFN-α9. The antiviral efficacy was dose-dependent and correlated with the induction of the IFN-inducible, antiviral genes, 2′–5′ oligoadenylate synthetase (OAS) and double-stranded RNA-dependent protein kinase. In trigeminal ganglion cells deficient in the downstream effector molecule of the OAS pathway, RNase L, the antiviral state induced by IFN-β was lost.</description><subject>Animals</subject><subject>Antiviral Agents - deficiency</subject><subject>Antiviral Agents - genetics</subject><subject>Antiviral Agents - physiology</subject><subject>Cell Line</subject><subject>Cells, Cultured</subject><subject>Cercopithecus aethiops</subject><subject>Endoribonucleases - deficiency</subject><subject>Endoribonucleases - genetics</subject><subject>Endoribonucleases - physiology</subject><subject>Female</subject><subject>Gene Expression Regulation, Viral - immunology</subject><subject>Herpes simplex virus</subject><subject>Herpes simplex virus 1</subject><subject>Herpesvirus 1, Human - genetics</subject><subject>Herpesvirus 1, Human - immunology</subject><subject>HSV-1</subject><subject>IFN-α</subject><subject>IFN-β</subject><subject>Immunity, Innate - genetics</subject><subject>Immunophenotyping</subject><subject>Interferon-beta - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred ICR</subject><subject>Neuroimmunology</subject><subject>OAS</subject><subject>PKR</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - immunology</subject><subject>Transfection</subject><subject>Trigeminal Ganglion - cytology</subject><subject>Trigeminal Ganglion - enzymology</subject><subject>Trigeminal Ganglion - immunology</subject><subject>Trigeminal Ganglion - virology</subject><subject>Vero Cells</subject><subject>Virus Replication - genetics</subject><subject>Virus Replication - immunology</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUuO1DAQhi0EYpqBI4C8QrAIlO3ESTYgNOIxUgskHmvLbVcSo8QxdtLQW47EQTgTyXRrgNVsqqTyV39V-SfkIYNnDJh8_mkJRVaUvHoC4ikAZzKrb5ENq0qeVTlnt8nmGjkj91L6CsAKkdd3yRnjtSx4wTfk56WfMDYYR5_9_kXTHELElDDRDmNYUnJD6PEH3bs4JzodAlJGI4beGT250VPn6RRdi4Pzuqet9m2_lg32_cJ3cZzbjmpPP77XCek2sxjQW_QTDXrqvuvDfXKn0X3CB6d8Tr68ef354l22_fD28uLVNjN5nU8Za6wu0aAAU9iyBKabRnIDprLNLgdE21jUFTOVhNryHW9AcGFkyYSA0khxTl4cdcO8G9CaZYWoexWiG3Q8qFE79f-Ld51qx73KQYLkYhF4fBKI47cZ06QGl9Y7tcdxTqoUMhcVVDeCrGZFVdb1AhZH0MQxpYjN9TYM1GqzurJZrR4qEOrKZrX2Pfr3lL9dJ18X4OURwOVD9w6jSsahN2hdRDMpO7obRvwBSw280A</recordid><startdate>20030801</startdate><enddate>20030801</enddate><creator>Carr, Daniel J.J.</creator><creator>Al-khatib, Khaldun</creator><creator>James, Cassandra M.</creator><creator>Silverman, Robert</creator><general>Elsevier B.V</general><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>7T5</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20030801</creationdate><title>Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway</title><author>Carr, Daniel J.J. ; Al-khatib, Khaldun ; James, Cassandra M. ; Silverman, Robert</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-1fda7ece30c5d7701aff62c0c8dfb40eedfdea81c8609d2b2f0323c6713307c63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Antiviral Agents - deficiency</topic><topic>Antiviral Agents - genetics</topic><topic>Antiviral Agents - physiology</topic><topic>Cell Line</topic><topic>Cells, Cultured</topic><topic>Cercopithecus aethiops</topic><topic>Endoribonucleases - deficiency</topic><topic>Endoribonucleases - genetics</topic><topic>Endoribonucleases - physiology</topic><topic>Female</topic><topic>Gene Expression Regulation, Viral - immunology</topic><topic>Herpes simplex virus</topic><topic>Herpes simplex virus 1</topic><topic>Herpesvirus 1, Human - genetics</topic><topic>Herpesvirus 1, Human - immunology</topic><topic>HSV-1</topic><topic>IFN-α</topic><topic>IFN-β</topic><topic>Immunity, Innate - genetics</topic><topic>Immunophenotyping</topic><topic>Interferon-beta - physiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred ICR</topic><topic>Neuroimmunology</topic><topic>OAS</topic><topic>PKR</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - immunology</topic><topic>Transfection</topic><topic>Trigeminal Ganglion - cytology</topic><topic>Trigeminal Ganglion - enzymology</topic><topic>Trigeminal Ganglion - immunology</topic><topic>Trigeminal Ganglion - virology</topic><topic>Vero Cells</topic><topic>Virus Replication - genetics</topic><topic>Virus Replication - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carr, Daniel J.J.</creatorcontrib><creatorcontrib>Al-khatib, Khaldun</creatorcontrib><creatorcontrib>James, Cassandra M.</creatorcontrib><creatorcontrib>Silverman, Robert</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carr, Daniel J.J.</au><au>Al-khatib, Khaldun</au><au>James, Cassandra M.</au><au>Silverman, Robert</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2003-08-01</date><risdate>2003</risdate><volume>141</volume><issue>1</issue><spage>40</spage><epage>46</epage><pages>40-46</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>The induction of an antiviral state by type I interferons (IFN) was evaluated in primary trigeminal ganglion cell cultures using herpes simplex virus type 1 (HSV-1). Cells treated with mouse IFN-β consistently showed the greatest resistance to HSV-1 infection in comparison to cells treated with IFN-α1, IFN-α4, IFN-α5, IFN-α6, or IFN-α9. The antiviral efficacy was dose-dependent and correlated with the induction of the IFN-inducible, antiviral genes, 2′–5′ oligoadenylate synthetase (OAS) and double-stranded RNA-dependent protein kinase. In trigeminal ganglion cells deficient in the downstream effector molecule of the OAS pathway, RNase L, the antiviral state induced by IFN-β was lost.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>12965252</pmid><doi>10.1016/S0165-5728(03)00216-9</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE |
| subjects | Animals Antiviral Agents - deficiency Antiviral Agents - genetics Antiviral Agents - physiology Cell Line Cells, Cultured Cercopithecus aethiops Endoribonucleases - deficiency Endoribonucleases - genetics Endoribonucleases - physiology Female Gene Expression Regulation, Viral - immunology Herpes simplex virus Herpes simplex virus 1 Herpesvirus 1, Human - genetics Herpesvirus 1, Human - immunology HSV-1 IFN-α IFN-β Immunity, Innate - genetics Immunophenotyping Interferon-beta - physiology Mice Mice, Inbred C57BL Mice, Inbred ICR Neuroimmunology OAS PKR Signal Transduction - genetics Signal Transduction - immunology Transfection Trigeminal Ganglion - cytology Trigeminal Ganglion - enzymology Trigeminal Ganglion - immunology Trigeminal Ganglion - virology Vero Cells Virus Replication - genetics Virus Replication - immunology |
| title | Interferon-β suppresses herpes simplex virus type 1 replication in trigeminal ganglion cells through an RNase L-dependent pathway |
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