[Epstein-Barr virus (EBV) infection associated with nasopharyngeal carcinoma]

Etiopathogenesis of nasopharyngeal carcinoma (NPC) is not fully understood yet. However, extensive research in this area has produced significant observations which facilitate the elucidation of the etiological factors and pathogenesis. A. Etiological Factors (a) EBV: EBV serological profiles in NPC patients, presence of EBV fingerprints in NPC tumor cells, and similar terminal repeat copies of EBV-DNA in NPC tissues strongly suggest the etiological role of EBV in NPC. (b) Genetic: Evidence supporting the genetic role in the etiology of NPC are mainly epidemiological. Although HLA studies have shown an increased relative risk in Chinese with A2, and BW 46 and in Malays with B17 and B18, the significance is not high. (c) Other environmental factors: In vitro studies have indicated the possibility of factors such as salted fish, dry fish, fermented vegetables, processed meat and some Chinese traditional herbal medicines. (d) Depressed cell-mediated immunity (CMI): While humoral antibodies to various EBV antigens are raised, the CMI seems to be lowered in NPC. It is not known, however, whether depressed CMI is the effect or the cause of NPC. B. Pathogenesis (a) Receptors for EBV: The receptors for EBV, C3d receptors, exist on cells of the basal layers which are undergoing metaplastic or hyperplastic change. These cells are close to the underlying stroma which contain the lymphocytes harbouring EBV. A pre-NPC stage of metaplasia/hyperplasia and sero epidemiological studies show raised EBV antibody titer 3-5 years before the development of NPC. (b) All NPC originate from the fossa of Rosenmüller which is a recessed depression behind the torus tubarius. This space can permit prolonged contact between environmental agents and the epithelial cells.