Epstein-Barr virus-epithelial cell interaction and its implication in the etiology of nasopharyngeal carcinoma.
The etiological role of EBV in NPC is still a matter for debate. A major question is how the viral DNA becomes associated with the carcinoma cell, since only B lymphocytes are at present known to have receptors to EBV. The following hypotheses are proposed: (1) The epithelial cells of the nasopharynx have EBV receptors in vivo; transformation of the epithelial cell thus results from a direct interaction between EBV and this cell type. The epithelial cells of the nasopharynx are not permissive for EBV infection. In this case: (2) Malignant or premalignant changes in the epithelial cells are required for EBV infection to take place. Thus, EBV may act either as a passive passenger or as an active promoter in NPC development. Or, (3) infection of the epithelial cells results from a specific interaction (involving either transfection or hybrid formation) between an EBV-infected B lymphocyte and an epithelial cell within the nasopharynx. Here again, the virus may either be passive or act as an oncogenic factor. Recent data are presented both for and against these hypotheses.
D000956:Antigens, Viral; D002277:Carcinoma / Q000209:etiology*; D002459:Cell Fusion; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D004279:DNA, Viral; D004847:Epithelial Cells; D004848:Epithelium / Q000276:immunology; D005814:Genes, Viral; D004854:Herpesvirus 4, Human / Q000276:immunology / Q000502:physiology*; D006801:Humans; D008214:Lymphocytes / Q000166:cytology; D009303:Nasopharyngeal Neoplasms / Q000209:etiology*; D009305:Nasopharynx / Q000166:cytology* / Q000276:immunology; D014779:Virus Replication
D000956:Antigens, Viral; D004279:DNA, Viral