Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
Lymphoma in human immunodeficiency virus infection.
Diss Abstr Int [B]; 54(12):6127 1994. Unique Identifier : AIDSLINE ICDB/95607173 Boyle MJ; Univ. of New South Wales, Australia
Abstract:
A clinical series of 41 HIV-associated NHL cases was analyzed. The findings confirmed, in an Australian population many features of HIV-associated NHL reported in other countries and suggested two definable groups of lymphoma patients: One with large cell immunoblastic histology, advanced immunodeficiency and a poor survival and another with small, noncleaved cell lymphoma, better preserved immune function and improved survival. To determine whether etiological factors may explain the patient survival differences, 20 HIV-associated NHL biopsies were investigated for HIV and EBV sequences using PCR. 10 samples (50%) harbored EBV, with 5 demonstrating A-type and 5 B-type EBV. HIV sequences were detected at an insignificant level. No patient had antibodies to HTLV-I. However, there was no survival difference between patients with A-type EBV, B-type EBV and without EBV in their tumors. The frequency of B-type EBV suggested B-type virus may be associated with immunodeficiency-associated lymphomas. This hypothesis was strengthened by assessing the EBV subtype in 30 Hodgkin's disease biopsies. Nine of the 30 cases had EBV in their malignant cells by in situ hybridization, 7 of A-type and 2 of B-type by PCR. The 2 B-type EBV cases had features suggesting immunodeficiency. To further explore EBV's role in HIV-associated NHL, 10 PGL cases were assessed for EBV and HIV sequences by PCR. HIV and EBV sequences were difficult to detect, suggesting direct infection of B cells by these viruses was not common in PGL. There followed studies to address whether the mechanisms of B cell activation in HIV infection contributed to lymphomagenesis, particularly the malignant transformation of EBV-infected B cells. The expression of IL-1, IL-2, IL-4, IL-5, IL-6, IL-10, TNF-a and IFN-g was similar in both HIV and control reactive lymph nodes, as determined by PCR. The increased NHL incidence in HIV infection is thus probably not due to the profile of local cytokine production in PGL, though prolonged exposure of B cells to stimulatory cytokines may still be a key factor. The thesis advances a number of significant concepts in the study of immunodeficiency-associated and HIV-associated NHL, providing an important insight into the mechanisms of lymphomagenesis in these conditions. (Full text NOT AVAILABLE FROM UNIVERSITY MICROFILMS INT'L.)
Keywords: Cytokines/METABOLISM Herpesvirus 4, Human Human HIV Infections/*COMPLICATIONS/METABOLISM In Situ Hybridization Lymphoma, Non-Hodgkin's/*COMPLICATIONS/METABOLISM/VIROLOGY Polymerase Chain Reaction THESIS 950430
M9541138
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Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
