The immunohistology of lymph nodes in HIV infection: a review

Abstract

Most available evidence indicates that lymph node immunohistologic alterations in HIV-infected patients represent a dynamic process characterized by an initial florid follicular hyperplasia that ultimately progresses to a burned-out, lymphocyte depletion end-point. During this process, HIV-infected cells appear to traffic through the lymph node, and the germinal center serves as a reservoir relatively rich in HIV antigens and intact virus. The localization of HIV within the germinal center may provide one stimulus for the florid follicular hyperplasia typical of early HIV-related lymphadenopathy and may play a role in follicle lysis, a process whereby the accessory cell FDC network of follicles undergoes disruption, which may in turn be responsible for the eventual disappearance of B-cell follicles in late-stage disease. Lymph node CD4+ T cells are selectively depleted with an initial preferential loss of the CD4+ subset concerned with B-cell differentiation. The expression of the CD4 antigen by various other cell types including monocytes, macrophages, histiocytic dendritic cells, and FDC provides one explanation as to why these cells are subject to HIV infection. Except perhaps in end-stage disease, alterations among various lymph node cell subsets do not correlate well with those in the peripheral blood. The latter is therefore regarded as a more sensitive parameter of progressive immunologic changes in HIV infection.