Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
IMMUNOPATHOLOGIC MECHANISMS OF HUMAN IMMUNODEFICIENCY VIRUS (HIV) INFECTION
The Human Retroviruses. Gallo RC and Jay G, eds. San Diego, Academic Press, p. 141-61, 1991.. Unique Identifier : AIDSLINE ICDB/92678725 Rosenberg ZF; Fauci AS; Natl. Inst. of Allergy and Infectious Diseases, NIH, Bethesda, MD; 20892
Abstract:
The most striking feature of infection with HIV in vivo is a dramatic reduction in the number of T4 cells, a specific subset of helper/inducer T lymphocytes that expresses the CD4 antigen. The ultimate destruction of the T4 cell population results in a critical immune deficiency that permits the development of a wide range of opportunistic infections and tumors. Immunopathology of HIV infection is reviewed, including mechanisms of T4 cell depletion (CD4 receptor in HIV infection, direct virus-induced T4 cell cytopathicity, indirect methods of T4 cell cytopathicity); impairment of immune system function (functional abnormalities of T4 cells, effects of HIV on other immune cells, and HIV infection of other cell types); role of the monocyte/macrophage in HIV infection; mechanisms of HIV-induced neurological disease; activation of latent HIV infection; and subversion of the immune system by HIV. It is becoming increasingly clear that initial infection with HIV and activation of HIV from a latent to a productive infection is intrinsically involved with the functioning of the human immune system. Activation of T cells has been correlated with the production of a cellular protein, NFkappaB, which binds to specific sites in the HIV promoter and is involved in the initiation of viral RNA transcription. NFkappaB also is important in HIV expression in monocytes/macrophages because monocyte differentiation is associated both with the appearance of NFkappaB-binding activity, which is constitutively produced in mature monocyte/macrophages, and with HIV replication. Tumor necrosis factor-alpha (TNF-alpha) has been shown to be present in significant levels in the sera of patients with AIDS. A recent study showed that the binding of HIV to the CD4 receptor on monocyte/macrophages results in the induction of TNF-alpha. Higher numbers of TNF-alpha receptors are present on the surface of HIV-infected cells when compared to their infected counterparts. Thus, TNF-alpha may alone, or in synergy with other cytokines, function in an autocrine/paracrine loop to enhance replication of HIV and facilitate spread of virus to uninfected cells. If this proves correct in vivo, HIV will have been shown to subvert the usual mechanisms of cytokine-induced immunological activation to its own advantage. (141 Refs)
Keywords: Animal Antigens, CD4/IMMUNOLOGY AIDS Dementia Complex/IMMUNOLOGY Cell Transformation, Viral/IMMUNOLOGY CD4-Positive T-Lymphocytes/*IMMUNOLOGY/MICROBIOLOGY Human HIV/*IMMUNOLOGY/PATHOGENICITY HIV Infections/*IMMUNOLOGY Virus Activation/IMMUNOLOGY MONOGRAPH REVIEW
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Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
