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Neurological Aspects of Human Immunodeficiency Virus Infection

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Neuropathogenic Viruses and Immunity

Part of the book series: Infectious Agents and Pathogenesis ((IAPA))

Abstract

The human immunodeficiency virus (HIV), the etiologic agent of the acquired immune deficiency syndrome (AIDS),1–3 belongs to a taxonomic group of nononcogenic retroviruses termed lentivirinae that share biological, biochemical, and molecular features for viral persistence.4–11 The hallmark of HIV infection is a relentless and profound immunosuppression mediated by a selective depletion of helper/inducer T lymphocytes.12–15 However, the virus-infected macrophage is also intimately involved in HIV pathogenesis. Primary HIV-induced disease revolves around a near-exclusive replication of virus in multinucleated and mono-nucleated macrophages typified by central nervous system (CNS) infection.16-24 Brain macrophages are likely infected soon after viral exposure22–25 and contribute to CNS-related neuronal injury through the secretion of neurotoxins (of viral or cellular origin) and/or by coexistent opportunistic infections. Indeed, the highest levels of HIV gene expression found in brain macrophages are associated with clinical disease in infected individuals.25 The mechanisms by which HIV infection results in immunosuppression and progressive neurological disease are the primary focus of this chapter.

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Gendelman, H.E., Gendelman, S. (1992). Neurological Aspects of Human Immunodeficiency Virus Infection. In: Specter, S., Bendinelli, M., Friedman, H. (eds) Neuropathogenic Viruses and Immunity. Infectious Agents and Pathogenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5886-2_12

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