| Literature DB >> 6101750 |
Abstract
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.Entities:
Mesh:
Substances:
Year: 1980 PMID: 6101750 DOI: 10.1016/s0140-6736(80)90792-8
Source DB: PubMed Journal: Lancet ISSN: 0140-6736 Impact factor: 79.321