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Immunological Dysregulation of Lymph Nodes in AIDS Patients

  • G. R. F. Krueger
  • D. V. Ablashi
  • P. Lusso
  • S. F. Josephs
Part of the Current Topics in Pathology book series (CT PATHOLOGY, volume 84/2)

Abstract

Acquired immune deficiency syndrome (AIDS) is characterized by a progressive loss in T lymphocytes with CD4 phenotype. This cell represents one of the major components in the immune regulatory network controlling the function not only of the immune system itself but also of macrophages and of natural killer cells as well as the proliferation of hematopoietic stem cells and of fibroblasts. CD4 cell loss will result in rather complex and individually variable defects in host defense and cell proliferation. The consequence of such defects are recurrent infections by opportunists and other agents and uncontrolled cell proliferation in the immune system and in other cells with ultimate death from infections or neoplasia. Since the human immune deficiency virus HIV-1 (formerly HTLV-III, LAV-1) was detected in patients with AIDS and was identified to cause lytic infections in CD4 lymphocytes, this virus is regarded as the etiological agent of AIDS (Gallo et al. 1983, 1985; Barre-Sinoussi et al. 1983; Montagnier 1986). There are, however, a number of phenomena in AIDS which are not readily explained by HIV-1 infection alone (Duesberg 1987), so that a search for additional mechanisms contributing to the pathogenesis of the disease seems warranted (Purtilo et al. 1985 a; Krueger 1986 b). Even if HIV-1 should ultimately prove to be the sole etiopathogenic agent, lytic infection of CD4 cells alone can hardly explain the entire functional defect in this cell population. Critical analysis of all parameters of immune deficiency developing during the course of AIDS is thus indicated and may provide further clues as to the complex pathogenesis of the disease.

Keywords

Human Immunodeficiency Virus Human Immunodeficiency Virus Type Acquire Immune Deficiency Syndrome Immune Deficiency Syndrome Postcapillary Venule 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer-Verlag Berlin Heidelberg 1991

Authors and Affiliations

  • G. R. F. Krueger
  • D. V. Ablashi
  • P. Lusso
  • S. F. Josephs

There are no affiliations available

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