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We examined IgG and IgA antibody responses against 202 protein sequences representing 86 EBV proteins using a microarray and sera from 139 EBV\u2010positive cHL cases, 70 EBV\u2010negative cHL cases and 141 population\u2010based controls frequency matched to EBV\u2010positive cHL cases on sex and age by area (UK, Denmark and Sweden). We leveraged existing data on the proportion of circulating B\u2010cells infected by EBV and levels of serum CCL17, a chemokine secreted by cHL tumor cells, from a subset of the cHL cases in the UK. Total IgG but not IgA response level was significantly different between EBV\u2010positive cHL cases and controls. The distinct serological response included significant elevations in 16 IgG antibodies and 2 IgA antibodies, with odds ratios<jats:sub>highest <jats:italic>vs<\/jats:italic>. lowest tertile\u2009&gt;\u20093<\/jats:sub> observed for the following EBV proteins: LMP1 (oncogene), BcLF1 (VCAp160, two variants) and BBLF1 (two variants). Our cHL IgG signature correlated with the proportion of circulating EBV\u2010infected B\u2010cells, but not serum CCL17 levels. We observed no differences in the anti\u2010EBV antibody profile between EBV\u2010negative cHL cases and controls. BdRF1(VCAp40)\u2010IgG and BZLF1(Zta)\u2010IgG were identified as the serological markers best able to distinguish EBV\u2010positive from EBV\u2010negative cHL tumors. Our results support the hypothesis that differences in the EBV antibody profile are specific to patients with EBV\u2010positive cHL and are not universally observed as part of a systematically dysregulated immune response present in all cHL cases.<\/jats:p>","DOI":"10.1002\/ijc.32741","type":"journal-article","created":{"date-parts":[[2019,10,16]],"date-time":"2019-10-16T22:31:02Z","timestamp":1571265062000},"page":"608-618","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Evaluation of the antibody response to the EBV proteome in EBV\u2010associated classical Hodgkin lymphoma"],"prefix":"10.1002","volume":"147","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0136-651X","authenticated-orcid":false,"given":"Zhiwei","family":"Liu","sequence":"first","affiliation":[{"name":"Division of Cancer Epidemiology and Genetics National Cancer Institute  Rockville MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruth F.","family":"Jarrett","sequence":"additional","affiliation":[{"name":"MRC\u2010University of Glasgow Centre for Virus Research  Glasgow United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Hjalgrim","sequence":"additional","affiliation":[{"name":"Statens Serum Institut  Copenhagen Denmark"},{"name":"Department of Haematology Rigshospitalet  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carla","family":"Proietti","sequence":"additional","affiliation":[{"name":"Centre for Molecular Therapeutics, Australian Institute of Tropical Health &amp; Medicine James Cook University  Cairns QLD Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen T.","family":"Chang","sequence":"additional","affiliation":[{"name":"Stanford Cancer Institute  Stanford CA"},{"name":"Center for Health Sciences Exponent, Inc.  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