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Department of Community Health Sciences, University of Edinburgh Medical School, Edinburgh EH8 9AG [F. E. A.]; Leukaemia Research Fund Virus Centre, Department of Veterinary Pathology, Glasgow G61 1QH [R. F. J., A. A. A., D. G.]; Leukaemia Research Fund, Centre for Clinical Epidemiology, UMV Leeds, Leeds LS2 9NG [R. A. C., E. K.]; Clinical Trials and Statistics Unit, Institute of Cancer Research, Sutton, Surrey SM2 5NG [D. A. G., D. J. L.]; and Immunogenetics Laboratory, University of Manchester, St. Marys Hospital, Manchester M13 0JH [G. M. T.], United Kingdom
Cases of Hodgkins disease (HD) may be distinguished by whether they do [EBV-positive (+ve) cases] or do not [EBV-negative (-ve) cases] have evidence of EBV DNA in the Reed-Sternberg cells. Only one study has attempted to distinguish epidemiological risk factors for EBV+ve and EBV-ve HD, and none have compared inherited susceptibility. The present study involves a population-based case series of HD, diagnosed in patients between 1624 years of age in the United Kingdom (n = 118), of whom 87% were classified by EBV status (EBV+ve, 19, EBV-ve, 84). History of infectious illness, EBV antibody titers, and HLA-DPB1 type have been compared in EBV+ve and EBV-ve cases. Reported infectious mononucleosis was more frequent in EBV+ve cases (odds ratio (OR), 5.10; 95% confidence interval (CI), 1.1224.4). EBV antibody titers to viral capsid antigen were significantly higher in EBV+ve cases (P for trend = 0.02). Higher proportions of EBV+ve (43%) than EBV-ve (31%) cases typed positive for HLA-DPB1*0301, but this was not statistically significant; the association of infectious mononucleosis with EBV+ve cases was stronger in this HLA subgroup (OR, 17.1; 95%CI, 1.061177) than in other cases (OR, 1.24; 95% CI, 0.0215.4). Although these results are based on small numbers of HD cases, they provide suggestive evidence that the etiology of EBV+ve HD may involve inherited susceptibility to EBV.
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