EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment
Identifieur interne : 000E58 ( Istex/Corpus ); précédent : 000E57; suivant : 000E59EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment
Auteurs : Mattias Magnusson ; Mikael Brisslert ; Kiandoht Zendjanchi ; Magnus Lindh ; Maria I. BokarewaSource :
- Rheumatology [ 1462-0324 ] ; 2010-10.
Abstract
Objectives. Viruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients. Methods. Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion. Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months. Results. Before RTX treatment, EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus. Parvovirus was further detected in eight patients (parvo-positive group). Twelve patients were negative for the analysed viruses. Following RTX, EBV was cleared, whereas parvovirus was unaffected. Eighteen patients were responders, of which 12 were EBV positive. The decrease in the DAS-28 was significantly higher in EBV-positive group compared with parvo-positive group (P0.002) and virus-negative patients (P0.04). Most of EBV-negative patients that responded to RTX (75) required retreatment within the following 11 months compared with only 8 of responding EBV-positive patients. A decrease of RF, Ig-producing cells and CD19 B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups. Conclusions. EBV and parvovirus genomes are frequently found in bone marrow of RA patients. The presence of EBV genome was associated with a better clinical response to RTX. Thus, presence of EBV genome may predict clinical response to RTX.
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DOI: 10.1093/rheumatology/keq159
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</title><author><name sortKey="Magnusson, Mattias" sort="Magnusson, Mattias" uniqKey="Magnusson M" first="Mattias" last="Magnusson">Mattias Magnusson</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: mattias.magnusson@rheuma.gu.se</mods:affiliation></affiliation></author><author><name sortKey="Brisslert, Mikael" sort="Brisslert, Mikael" uniqKey="Brisslert M" first="Mikael" last="Brisslert">Mikael Brisslert</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Zendjanchi, Kiandoht" sort="Zendjanchi, Kiandoht" uniqKey="Zendjanchi K" first="Kiandoht" last="Zendjanchi">Kiandoht Zendjanchi</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Lindh, Magnus" sort="Lindh, Magnus" uniqKey="Lindh M" first="Magnus" last="Lindh">Magnus Lindh</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Bokarewa, Maria I" sort="Bokarewa, Maria I" uniqKey="Bokarewa M" first="Maria I." last="Bokarewa">Maria I. Bokarewa</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:26802C2D90D57A715C17F8AF434738E0BED971D1</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1093/rheumatology/keq159</idno><idno type="url">https://api.istex.fr/document/26802C2D90D57A715C17F8AF434738E0BED971D1/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000E58</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</title><author><name sortKey="Magnusson, Mattias" sort="Magnusson, Mattias" uniqKey="Magnusson M" first="Mattias" last="Magnusson">Mattias Magnusson</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: mattias.magnusson@rheuma.gu.se</mods:affiliation></affiliation></author><author><name sortKey="Brisslert, Mikael" sort="Brisslert, Mikael" uniqKey="Brisslert M" first="Mikael" last="Brisslert">Mikael Brisslert</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Zendjanchi, Kiandoht" sort="Zendjanchi, Kiandoht" uniqKey="Zendjanchi K" first="Kiandoht" last="Zendjanchi">Kiandoht Zendjanchi</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Lindh, Magnus" sort="Lindh, Magnus" uniqKey="Lindh M" first="Magnus" last="Lindh">Magnus Lindh</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author><author><name sortKey="Bokarewa, Maria I" sort="Bokarewa, Maria I" uniqKey="Bokarewa M" first="Maria I." last="Bokarewa">Maria I. Bokarewa</name><affiliation><mods:affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Rheumatology</title><idno type="ISSN">1462-0324</idno><idno type="eISSN">1462-0332</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-10">2010-10</date><biblScope unit="volume">49</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1911">1911</biblScope><biblScope unit="page" to="1919">1919</biblScope></imprint><idno type="ISSN">1462-0324</idno></series><idno type="istex">26802C2D90D57A715C17F8AF434738E0BED971D1</idno><idno type="DOI">10.1093/rheumatology/keq159</idno><idno type="ArticleID">keq159</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1462-0324</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Objectives. Viruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients. Methods. Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion. Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months. Results. Before RTX treatment, EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus. Parvovirus was further detected in eight patients (parvo-positive group). Twelve patients were negative for the analysed viruses. Following RTX, EBV was cleared, whereas parvovirus was unaffected. Eighteen patients were responders, of which 12 were EBV positive. The decrease in the DAS-28 was significantly higher in EBV-positive group compared with parvo-positive group (P0.002) and virus-negative patients (P0.04). Most of EBV-negative patients that responded to RTX (75) required retreatment within the following 11 months compared with only 8 of responding EBV-positive patients. A decrease of RF, Ig-producing cells and CD19 B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups. Conclusions. EBV and parvovirus genomes are frequently found in bone marrow of RA patients. The presence of EBV genome was associated with a better clinical response to RTX. Thus, presence of EBV genome may predict clinical response to RTX.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Mattias Magnusson</name><affiliations><json:string>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</json:string><json:string>E-mail: mattias.magnusson@rheuma.gu.se</json:string></affiliations></json:item><json:item><name>Mikael Brisslert</name><affiliations><json:string>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</json:string></affiliations></json:item><json:item><name>Kiandoht Zendjanchi</name><affiliations><json:string>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</json:string></affiliations></json:item><json:item><name>Magnus Lindh</name><affiliations><json:string>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</json:string></affiliations></json:item><json:item><name>Maria I. Bokarewa</name><affiliations><json:string>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Clinical Science</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Rheumatoid arthritis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Biological therapy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>B-cell depletion</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Viral infection</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>EpsteinBarr virus</value></json:item></subject><articleId><json:string>keq159</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Objectives. Viruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients. Methods. Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion. Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months. Results. Before RTX treatment, EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus. Parvovirus was further detected in eight patients (parvo-positive group). Twelve patients were negative for the analysed viruses. Following RTX, EBV was cleared, whereas parvovirus was unaffected. Eighteen patients were responders, of which 12 were EBV positive. The decrease in the DAS-28 was significantly higher in EBV-positive group compared with parvo-positive group (P0.002) and virus-negative patients (P0.04). Most of EBV-negative patients that responded to RTX (75) required retreatment within the following 11 months compared with only 8 of responding EBV-positive patients. A decrease of RF, Ig-producing cells and CD19 B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups. Conclusions. EBV and parvovirus genomes are frequently found in bone marrow of RA patients. The presence of EBV genome was associated with a better clinical response to RTX. Thus, presence of EBV genome may predict clinical response to RTX.</abstract><qualityIndicators><score>8.5</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612.283 x 790.866 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1734</abstractCharCount><pdfWordCount>5416</pdfWordCount><pdfCharCount>35537</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>259</abstractWordCount></qualityIndicators><title>EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</title><genre><json:string>research-article</json:string></genre><host><volume>49</volume><publisherId><json:string>brheum</json:string></publisherId><pages><last>1919</last><first>1911</first></pages><issn><json:string>1462-0324</json:string></issn><issue>10</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1462-0332</json:string></eissn><title>Rheumatology</title></host><categories><wos><json:string>RHEUMATOLOGY</json:string></wos></categories><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1093/rheumatology/keq159</json:string></doi><id>26802C2D90D57A715C17F8AF434738E0BED971D1</id><score>0.24932158</score><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/26802C2D90D57A715C17F8AF434738E0BED971D1/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/26802C2D90D57A715C17F8AF434738E0BED971D1/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/26802C2D90D57A715C17F8AF434738E0BED971D1/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>The Author(s) 2010. Published by Oxford University Press on behalf of The British Society for Rheumatology.</p></availability><date>2010-06-14</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</title><author xml:id="author-1" corresp="yes"><persName><forename type="first">Mattias</forename><surname>Magnusson</surname></persName><email>mattias.magnusson@rheuma.gu.se</email><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation></author><author xml:id="author-2"><persName><forename type="first">Mikael</forename><surname>Brisslert</surname></persName><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation></author><author xml:id="author-3"><persName><forename type="first">Kiandoht</forename><surname>Zendjanchi</surname></persName><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation></author><author xml:id="author-4"><persName><forename type="first">Magnus</forename><surname>Lindh</surname></persName><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation></author><author xml:id="author-5"><persName><forename type="first">Maria I.</forename><surname>Bokarewa</surname></persName><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation></author></analytic><monogr><title level="j">Rheumatology</title><idno type="pISSN">1462-0324</idno><idno type="eISSN">1462-0332</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2010-10"></date><biblScope unit="volume">49</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1911">1911</biblScope><biblScope unit="page" to="1919">1919</biblScope></imprint></monogr><idno type="istex">26802C2D90D57A715C17F8AF434738E0BED971D1</idno><idno type="DOI">10.1093/rheumatology/keq159</idno><idno type="ArticleID">keq159</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010-06-14</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Objectives. Viruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients. Methods. Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion. Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months. Results. Before RTX treatment, EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus. Parvovirus was further detected in eight patients (parvo-positive group). Twelve patients were negative for the analysed viruses. Following RTX, EBV was cleared, whereas parvovirus was unaffected. Eighteen patients were responders, of which 12 were EBV positive. The decrease in the DAS-28 was significantly higher in EBV-positive group compared with parvo-positive group (P0.002) and virus-negative patients (P0.04). Most of EBV-negative patients that responded to RTX (75) required retreatment within the following 11 months compared with only 8 of responding EBV-positive patients. A decrease of RF, Ig-producing cells and CD19 B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups. Conclusions. EBV and parvovirus genomes are frequently found in bone marrow of RA patients. The presence of EBV genome was associated with a better clinical response to RTX. Thus, presence of EBV genome may predict clinical response to RTX.</p></abstract><textClass><keywords scheme="keyword"><list><item><term>Clinical Science</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>Rheumatoid arthritis</term></item><item><term>Biological therapy</term></item><item><term>B-cell depletion</term></item><item><term>Viral infection</term></item><item><term>EpsteinBarr virus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-06-14">Created</change><change when="2010-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/26802C2D90D57A715C17F8AF434738E0BED971D1/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">rheumatology</journal-id><journal-id journal-id-type="publisher-id">brheum</journal-id><journal-title>Rheumatology</journal-title><issn pub-type="ppub">1462-0324</issn><issn pub-type="epub">1462-0332</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/rheumatology/keq159</article-id><article-id pub-id-type="publisher-id">keq159</article-id><article-categories><subj-group><subject>Clinical Science</subject></subj-group></article-categories><title-group><article-title>Epstein–Barr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Magnusson</surname><given-names>Mattias</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Brisslert</surname><given-names>Mikael</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Zendjanchi</surname><given-names>Kiandoht</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lindh</surname><given-names>Magnus</given-names></name><xref ref-type="aff" rid="AFF1"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Bokarewa</surname><given-names>Maria I.</given-names></name><xref ref-type="aff" rid="AFF1"><sup>1</sup></xref></contrib></contrib-group><aff id="AFF1"><sup>1</sup>Department of Rheumatology and Inflammation Research and <sup>2</sup>Department of Virology, Sahlgrenska University Hospital, Göteborg, Sweden.</aff><author-notes><corresp>Correspondence to: Mattias Magnusson, Department of Rheumatology and Inflammation Research, Sahlgrenska University Hospital, Guldhedsgatan 10A, 413 46 Göteborg, Sweden. E-mail:<email>mattias.magnusson@rheuma.gu.se</email></corresp></author-notes><pub-date pub-type="ppub"><month>10</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>14</day><month>6</month><year>2010</year></pub-date><volume>49</volume><issue>10</issue><fpage>1911</fpage><lpage>1919</lpage><history><date date-type="received"><day>1</day><month>10</month><year>2009</year></date><date date-type="rev-recd"><day>27</day><month>4</month><year>2010</year></date></history><permissions><copyright-statement>© The Author(s) 2010. Published by Oxford University Press on behalf of The British Society for Rheumatology.</copyright-statement><copyright-year>2010</copyright-year><license license-type="creative-commons" xlink:href="http://creativecommons.org/licenses/by-nc/2.5"><p>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</p></license></permissions><abstract><p><bold>Objectives</bold>. Viruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients.</p><p><bold>Methods.</bold> Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion. Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months.</p><p><bold>Results.</bold> Before RTX treatment, EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus. Parvovirus was further detected in eight patients (parvo-positive group). Twelve patients were negative for the analysed viruses. Following RTX, EBV was cleared, whereas parvovirus was unaffected. Eighteen patients were responders, of which 12 were EBV positive. The decrease in the DAS-28 was significantly higher in EBV-positive group compared with parvo-positive group (<italic>P</italic> = 0.002) and virus-negative patients (<italic>P</italic> = 0.04). Most of EBV-negative patients that responded to RTX (75%) required retreatment within the following 11 months compared with only 8% of responding EBV-positive patients. A decrease of RF, Ig-producing cells and CD19<sup>+</sup> B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups.</p><p><bold>Conclusions.</bold> EBV and parvovirus genomes are frequently found in bone marrow of RA patients. The presence of EBV genome was associated with a better clinical response to RTX. Thus, presence of EBV genome may predict clinical response to RTX.</p></abstract><kwd-group><kwd>Rheumatoid arthritis</kwd><kwd>Biological therapy</kwd><kwd>B-cell depletion</kwd><kwd>Viral infection</kwd><kwd>Epstein–Barr virus</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>EpsteinBarr virus in bone marrow of rheumatoid arthritis patients predicts response to rituximab treatment</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Mattias</namePart><namePart type="family">Magnusson</namePart><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation><affiliation>E-mail: mattias.magnusson@rheuma.gu.se</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mikael</namePart><namePart type="family">Brisslert</namePart><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kiandoht</namePart><namePart type="family">Zendjanchi</namePart><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Magnus</namePart><namePart type="family">Lindh</namePart><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maria I.</namePart><namePart type="family">Bokarewa</namePart><affiliation>Department of Rheumatology and Inflammation Research and Department of Virology, Sahlgrenska University Hospital, Gteborg, Sweden.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Clinical Science</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2010-10</dateIssued><dateCreated encoding="w3cdtf">2010-06-14</dateCreated><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Objectives. Viruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients. Methods. Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion. Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months. Results. Before RTX treatment, EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus. Parvovirus was further detected in eight patients (parvo-positive group). Twelve patients were negative for the analysed viruses. Following RTX, EBV was cleared, whereas parvovirus was unaffected. Eighteen patients were responders, of which 12 were EBV positive. The decrease in the DAS-28 was significantly higher in EBV-positive group compared with parvo-positive group (P0.002) and virus-negative patients (P0.04). Most of EBV-negative patients that responded to RTX (75) required retreatment within the following 11 months compared with only 8 of responding EBV-positive patients. A decrease of RF, Ig-producing cells and CD19 B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups. Conclusions. EBV and parvovirus genomes are frequently found in bone marrow of RA patients. The presence of EBV genome was associated with a better clinical response to RTX. Thus, presence of EBV genome may predict clinical response to RTX.</abstract><subject><genre>keywords</genre><topic>Rheumatoid arthritis</topic><topic>Biological therapy</topic><topic>B-cell depletion</topic><topic>Viral infection</topic><topic>EpsteinBarr virus</topic></subject><relatedItem type="host"><titleInfo><title>Rheumatology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1462-0324</identifier><identifier type="eISSN">1462-0332</identifier><identifier type="PublisherID">brheum</identifier><identifier type="PublisherID-hwp">rheumatology</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>49</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1911</start><end>1919</end></extent></part></relatedItem><identifier type="istex">26802C2D90D57A715C17F8AF434738E0BED971D1</identifier><identifier type="DOI">10.1093/rheumatology/keq159</identifier><identifier type="ArticleID">keq159</identifier><accessCondition type="use and reproduction" contentType="copyright">The Author(s) 2010. 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