Important note: Information in this article was accurate in 1985. The state of the art may have changed since the publication date.
EPSTEIN-BARR VIRUS - ONCOGENESIS IN IMMUNE DEFICIENT INDIVIDUALS
The Role of Viruses in Human Cancer. Volume II. Giraldo G, Beth E, eds. New York, Elsevier Science Publishers, p. 119-36, 1984.. Unique Identifier : AIDSLINE ICDB/85610751 Purtilo DT; Dept. of Pathology, Univ. of Nebraska Medical Center, 42nd and; Dewey Ave., Omaha, NE 68105
Abstract:
Epstein-Barr virus (EBV) isolated from patients (pts) with infectious mononucleosis (IM), Burkitt's lymphoma (BL), or nasopharyngeal carcinoma appears to constitute one strain, implying that host immune response, cofactors, and cytogenetic events govern the outcome of infection. Host defense against EBV includes natural killer cells, interferon from infected B-cells, T-cells, antibody, antibody-dependent cellular cytotoxicity, and memory T-cells. EBV-induced lymphoma is probably a multi-step process that includes thymic epithelial destruction, which has been reported in graft-versus-host reactions, X-linked lymphoproliferative syndrome (XLP), Steinbrinck-Chediak-Higashi syndrome, fatal IM, and the acquired immune deficiency syndrome (AIDS). The mechanism for destruction of thymic epithelium is unknown; malignant lymphoma (ML) may result from prolonged EBV-induced lymphocyte proliferation and chromosome breakage; altered karyotypes have been described in pts with fatal IM or AIDS. Monoclonal malignancies resembling BL are associated with AIDS, and AIDS lymph nodes often contain EBV. ML is the commonest malignancy of children with inherited immune deficiencies. XLP is characterized by a defect of T-lymphocytes, which results in chronic active EBV infection; all lymphomas in XLP belong to the B-cell lineage. Immunocompetence appears to be greater in XLP pts who develop ML than in those who succumb to IM, possibly because superior immunity permits polyclonal B-cell proliferation to continue long enough to allow conversion to monoclonal proliferation. Conversion of IM to ML has been reported in numerous cases of pts with inherited or acquired immune deficiency. EBV genome has also been found in MLs occurring in pts with ataxia telangiectasia, common variable immune deficiency and renal, cardiac, or thymic epithelial transplants. (35 Refs)
Keywords: Acquired Immunodeficiency Syndrome/IMMUNOLOGY Animal Antibody Formation B-Lymphocytes/IMMUNOLOGY Burkitt's Lymphoma/IMMUNOLOGY Cell Transformation, Neoplastic/*IMMUNOLOGY Cell Transformation, Viral Gene Expression Regulation Herpesvirus 4, Human/GENETICS/IMMUNOLOGY Hodgkin's Disease/IMMUNOLOGY Homosexuality Human Immunity, Cellular Immunologic Deficiency Syndromes/*IMMUNOLOGY Kidney/TRANSPLANTATION Kidney Transplantation Transplantation Immunology Tumor Virus Infections/*IMMUNOLOGY MEETING PAPER
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Important note: Information in this article was accurate in 1985. The state of the art may have changed since the publication date.
