Epstein-Barr-virus-induced oncogenesis in immune-deficient individuals.
Experimental and clinical evidence supports the notion that the Epstein-Barr virus (EBV) can become oncogenic in immune-deficient hosts. Renal transplant recipients and children with inherited immune deficiency are at high risk for lymphomagenesis. Defective immune responses to EBV permit persistence of polyclonal proliferation of B cells. Conversion from polyclonal to monoclonal proliferation is probably the result of a cytogenetic error in a B cell. This hypothesis can be tested prospectively in patients with immune deficiency by immunological, EBV, and genetic studies.
D000818:Animals; D000956:Antigens, Viral / Q000276:immunology; D001402:B-Lymphocytes / Q000473:pathology; D002051:Burkitt Lymphoma / Q000209:etiology / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D002648:Child; D002869:Chromosome Aberrations; D004854:Herpesvirus 4, Human; D006801:Humans; D007153:Immunologic Deficiency Syndromes / Q000150:complications*; D007244:Infectious Mononucleosis / Q000209:etiology / Q000276:immunology; D008223:Lymphoma / Q000209:etiology*; D008297:Male; D014412:Tumor Virus Infections / Q000276:immunology
D000956:Antigens, Viral