Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
PATHOLOGY AND IMMUNOHISTOLOGY OF LYMPH NODES IN HIV INFECTION
AIDS, Acquired Immune Deficiency Syndrome, and other Manifestations of HIV Infection. Wormser GP et al, eds. Park Ridge, NJ, Noyes Publications, p. 867-88, 1987.. Unique Identifier : AIDSLINE ICDB/88647013 Wood GS; Veterans Administration Medical Center, Stanford Univ. Medical; Center, Palo Alto, CA
Abstract:
Human immunodeficiency virus (HIV) infection can be asymptomatic, result in the persistent generalized lymphadenopathy syndrome (PGL) or other manifestations of AIDS-related complex, or result in AIDS. The variable clinical features of PGL and AIDS are reflected by the broad spectrum of histopathologic and immunohistologic alterations that have been observed in lymph nodes from these patients (pts). This chapter describes lymph node anatomy, reactive lymphadenopathy, neoplastic lymphadenopathy, clinical relevance of lymph node histopathology, follicle lysis, T-cell subsets, non-T cells, B-lineage cells, histiocytes (macrophages and dendritic cells), and natural killer and killer cells. The histopathologic findings associated with HIV infection fall into two major categories, reactive and neoplastic. The reactive changes consist predominantly of florid follicular hyperplasia or lymphocyte depletion. The neoplastic changes consist of Kaposi's sarcoma or lymphoma. Immunohistologic studies, interpreted in the context of in vitro studies of HIV infection, suggest certain pathogenetic mechanisms for the findings associated with PGL and AIDS. There appear to be at least two principal targets of HIV in lymph nodes, the T helper cells (TH) and follicular dendritic cells (FDC). Infection results in gradual depletion of CD4+Leu8+ TH associated with a reduced TH/T CS (cytotoxic-suppressor) ratio and impaired cell-mediated immunity. In this milieu of diminished host response, pts exhibit an increased incidence of opportunistic infections, Kaposi's sarcoma, and B-cell lymphoma. Transformation of tumor cells by cytomegalovirus or Epstein-Barr virus may be involved in the pathogenesis of these two neoplasms. Although peripheral blood T-cell subset alterations are often similar in PGL and AIDS, the absence of opportunistic infections and neoplasms in PGL may be related to the relative preservation of CF4+Leu8+ TH within the lymph node paracortex in PGL. Localization of HIV in or on FDC may play a role in the follicle lysis associated with PGL and AIDS. This architectural disruption of germinal centers might result in a disruption of FDC function, with deregulation of B-cell proliferation predisposing to B-cell lymphoma. In some cases, FDC may be destroyed eventually. This would be expected to result in regression of B-cell follicles, such as seen in lymph nodes exhibiting the lymphocyte depletion reactive pattern characteristic of preterminal AIDS, because FDC are an important component of the follicular micro environment. (72 Refs)
Keywords: Acquired Immunodeficiency Syndrome/*PATHOLOGY AIDS-Related Complex/*PATHOLOGY B-Lymphocytes/PATHOLOGY Human Immunohistochemistry Lymph Nodes/*PATHOLOGY Opportunistic Infections/PATHOLOGY Sarcoma, Kaposi's/PATHOLOGY Skin Neoplasms/PATHOLOGY T-Lymphocytes/PATHOLOGY MONOGRAPH REVIEW, TUTORIAL REVIEW
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Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
