Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
EPSTEIN-BARR VIRUS AND ACQUIRED IMMUNODEFICIENCY SYNDROME
Adv Viral Oncol; 8:203-17 1989. Unique Identifier : AIDSLINE ICDB/90659838 Ernberg I; Dept. of Tumor Biology, Karolinska Inst., Stockholm, Sweden
Abstract:
Next to T-helper lymphocytes, the Epstein-Barr virus (EBV)-carrying lymphoblasts were the second cell type shown to support HIV replication. The appearance of the oral hairy leukoplakias (OHLs), which can support EBV replication, is considered a bad prognostic sign in otherwise symptom-free HIV carriers. Approx one-fourth of the lymphomas in HIV carriers show the characteristic histopathology of Burkitt's lymphoma (BL). EBV in HIV carriers and in patients (pts) with AIDS is reviewed, including dysregulation of immune control of EBV in pts with AIDS (B-lymphocyte dysfunction, antibody titers to EBV antigens, EBV production in the oropharynx, increased spontaneous outgrowth, and EBV-specific cellular immunity in HIV carriers), HIV replication in EBV growth-transformed lymphoblasts, interaction between EBV and HIV at the molecular level, OHLs, increased risk of malignant lymphomas in pts with AIDS, EBV in BL and immunoblastic lymphomas, EBV in persistent generalized lymphadenopathy, and other EBV-dependent complications in AIDS. In HIV carriers, various signs of EBV activation can be detected that correlate crudely to the progress of the immune defect: increased oropharyngeal virus production, elevated antibody titers to EBV, increased circulating EBV-infected cells, and impaired T-cell immunity to the virus-infected cells. It is conceivable that this virus (re)activation results in an increased proliferation of EBV-infected B lymphocytes in vivo, which in turn increases the vulnerability of these cells and the risk that cytogenetic changes occur that determine the development of malignant clones. In addition to its role as a cofactor in lymphomas in pts with AIDS, EBV may be a cofactor to HIV in the pathogenesis of AIDS. EBV is ubiquitous in these pts; therefore, it is unlikely to be involved in triggering the progress of the immune defect. As the immune defect progresses, however, EBV may accelerate the process. Immune suppression could result in less control of EBV-infected lymphocytes, which proliferate in vivo, as in acute infectious mononucleosis. Second, an activation of the EBV-carrying B lymphocytes may result in a T-cell response, which could lead to more rapid recruitment of suitable activated T-cell targets for HIV, leading to their destruction. (76 Refs)
Keywords: Acquired Immunodeficiency Syndrome/GENETICS/IMMUNOLOGY/ *MICROBIOLOGY Antibodies, Viral/ANALYSIS B-Lymphocytes/IMMUNOLOGY Cell Transformation, Neoplastic/*GENETICS *Cell Transformation, Viral *Gene Expression Regulation, Viral Herpesvirus 4, Human/*GENETICS/IMMUNOLOGY Human Leukoplakia, Oral/MICROBIOLOGY Lymphoma/MICROBIOLOGY Male Tumor Virus Infections/GENETICS/IMMUNOLOGY/*MICROBIOLOGY Virus Activation JOURNAL ARTICLE REVIEW 912130
M91C4112
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Important note: Information in this article was accurate in 1991. The state of the art may have changed since the publication date.
