{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T14:31:21Z","timestamp":1793370681939,"version":"4.5.0"},"reference-count":112,"publisher":"American Society of Hematology","issue":"7","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Although a pathogenic role for the Epstein-Barr virus (EBV) is largely undisputed for tumors that are consistently EBV genome positive (eg, nasopharyngeal carcinoma, endemic Burkitt lymphoma), this is not the case for classical Hodgkin lymphoma (cHL), a tumor with only a variable EBV association. In light of recent developments in immunotherapeutics and small molecules targeting EBV, we believe it is now timely to reevaluate the role of EBV in cHL pathogenesis.<\/jats:p>","DOI":"10.1182\/blood.2019000568","type":"journal-article","created":{"date-parts":[[2019,6,11]],"date-time":"2019-06-11T21:35:21Z","timestamp":1560288921000},"page":"591-596","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":123,"title":["An etiological role for the Epstein-Barr virus in the pathogenesis of classical Hodgkin lymphoma"],"prefix":"10.1182","volume":"134","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0956-6468","authenticated-orcid":false,"given":"Paul G.","family":"Murray","sequence":"first","affiliation":[{"name":"Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom;"},{"name":"Health Research Institute, University of Limerick, Limerick, Ireland; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3919-4298","authenticated-orcid":false,"given":"Lawrence S.","family":"Young","sequence":"additional","affiliation":[{"name":"Warwick Medical School, University of Warwick, Coventry, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"issue":"23","key":"2020021109250333700_B1","doi-asserted-by":"crossref","first-page":"10962","DOI":"10.1073\/pnas.91.23.10962","article-title":"Hodgkin disease: Hodgkin and Reed-Sternberg cells picked from histological sections show clonal immunoglobulin gene rearrangements and appear to be derived from B cells at various stages of development","volume":"91","author":"K\u00fcppers","year":"1994","journal-title":"Proc Natl Acad Sci USA"},{"issue":"4","key":"2020021109250333700_B2","doi-asserted-by":"crossref","first-page":"1495","DOI":"10.1084\/jem.184.4.1495","article-title":"Hodgkin and Reed-Sternberg cells in Hodgkin\u2019s disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells","volume":"184","author":"Kanzler","year":"1996","journal-title":"J Exp Med"},{"issue":"2","key":"2020021109250333700_B3","doi-asserted-by":"crossref","first-page":"416","DOI":"10.1002\/1097-0142(197102)27:2<416::AID-CNCR2820270227>3.0.CO;2-W","article-title":"Elevated antibody titers to Epstein-Barr virus in Hodgkin\u2019s disease","volume":"27","author":"Levine","year":"1971","journal-title":"Cancer"},{"issue":"11","key":"2020021109250333700_B4","doi-asserted-by":"crossref","first-page":"689","DOI":"10.1056\/NEJM198903163201103","article-title":"Hodgkin\u2019s disease and Epstein-Barr virus. 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