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 persistenc...

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Veröffentlicht in:	The Lancet (British edition) 1980-02, Vol.1 (8163), p.300-303
1. Verfasser:	Purtilo, D T
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antigens, Viral - immunology B-Lymphocytes - pathology Burkitt Lymphoma - etiology Burkitt Lymphoma - genetics Burkitt Lymphoma - immunology Burkitt Lymphoma - pathology Child Chromosome Aberrations Herpesvirus 4, Human Humans Immunologic Deficiency Syndromes - complications Infectious Mononucleosis - etiology Infectious Mononucleosis - immunology Lymphoma - etiology Male Tumor Virus Infections - immunology
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Beschreibung
Zusammenfassung:	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.
ISSN:	0140-6736