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A case control study on immunity to two epstein‐barr virus‐associated antigens, and to herpes simplex virus and adenovirus in a population‐based group of patients with hodgkin's disease in denmark, 1971–73
Author(s) -
Hesse J.,
Ebbesen P.,
Levine P. H.,
Connelly R. R.,
Mordhorst C. H.
Publication year - 1977
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910190108
Subject(s) - virology , virus , herpes simplex virus , immunity , disease , antigen , population , immunology , medicine , herpesviridae , biology , viral disease , immune system , pathology , environmental health
One hundred and eighty‐five patients with untreated Hodgkin's disease (HD) comprising 86% of all new cases diagnosed in Denmark over a 2‐year period, were individually matched with healthy controls of the same age, sex and social class. In comparison to controls, HD patients showed significantly elevated mean antibody titres to Epstein‐Barr viral capsid antigen (EB‐VCA) and to herpes simplex virus, whereas no significant differences in mean titres were found for adenovirus common antigen. Subdivision of the patients by age, sex, social class, HL‐A antigens, stage of disease and histology did not alter this pattern, except that significant case‐control differences in EB‐VCA titres could be demonstrated only for the nodular sclerosis and lymphocyte predominance subgroups. After 1 year of treatment, a significant rise in EB‐VCA mean titre had taken place. Splenectomy seemed to promote this titre elevation. Neither the initial titres to EB‐VCA and EBV‐EA nor changes in titres over time were related to prognosis. The results of our study, which are more representative of a population of HD patients and controls than previously reported studies, confirm that the reported relationship between EBV and HD exists, but that the elevated EBV titres are probably not of etiologic significance in most HD patients.