ABSTRACT
Prior to the demonstration in situ of Epstein-Barr virus (EBV) genomes and antigens in Hodgkin’s lymphomas (HLs), several lines of evidence already pointed to the involvement of EBV in its pathogenesis. In particular, seroepidemiological investigations showed an increased risk of HL following infectious mononucleosis (IM) (1,2). Until the late 1980s, however, attempts had failed to unequivocally demonstrate EBV particles or gene products in HL tissues. Methodological advancements and development of EBV-specific probes and monoclonal antibodies made it possible to establish a firm association of EBV with HL. In 1997, a working group of the International Agency for Research on Cancer categorized the EBV as a group I carcinogen and concluded that there was sufficient evidence to consider the association between EBV and HL as causal (3).
