Role of Epstein-Barr virus in the etiology of Burkitt's lymphoma.

摘要: Although Epstein-Barr virus (EBV) was discovered in cultured Burkitt's lymphoma (BL) cells, its exact role remains unclear. Viral genome is found 95-98% of endemic BL and 15-20% non-endemic BL. Children destined to develop Africa show elevated titres viral capsid antibodies one two years preceding emergence A multistep process follows early EBV infection during childhood. Immune deficiency probably permits continuation the infections, with smouldering polyclonal B-cell proliferation proceeding. Final steps pathogenesis consist cytogenetic molecular conversion monoclonal Reciprocal chromosomal translocations involve breakpoints containing c-myc, heavy- light-chain Ig loci. Activation oncogenes, c-myc B-lym, may be essential spectrum EBV-induced pathological entities individuals X-linked lymphoproliferative acquired immune syndromes. Lymphoma identical occurs these immune-deficient patients. Non-endemic possibly due defects, initiators promoters proliferation, which not factors BL; however, events activation oncogenes pathways both