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Apoptosis and HIV neuropathogenesis

M G Espey1

  • 1Biology Department, Georgetown University, Washington, DC 20057, USA.

Medical Hypotheses
|June 1, 1995
PubMed
Summary

Human immunodeficiency virus (HIV) infection can cause brain dysfunction. A new hypothesis suggests T lymphocyte apoptosis aids HIV entry and spread in the central nervous system (CNS).

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Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • Human immunodeficiency virus (HIV) infection can lead to neurological dysfunction.
  • The mechanisms of HIV's central nervous system (CNS) tropism and dissemination are not fully understood.
  • Current theories propose HIV enters the brain via infected monocytes.

Purpose of the Study:

  • To present an alternative hypothesis for HIV entry and dissemination in the CNS.
  • To explore the role of T lymphocyte apoptosis in HIV neuropathogenesis.

Main Methods:

  • Review of existing observations regarding T lymphocyte apoptosis and HIV.
  • Analysis of HIV's presence and form within the CNS.
  • In vitro studies on macrophage infection by HIV-infected apoptotic T lymphocytes.

Main Results:

  • T lymphocyte apoptosis may be a CNS-specific inflammatory control mechanism.
  • T lymphocytes are the primary circulating reservoir of HIV.
  • Macrophages can become productively infected after phagocytizing HIV-infected apoptotic T lymphocytes in vitro.
  • Unintegrated HIV is the predominant form in the CNS.

Conclusions:

  • Aberrantly high T lymphocyte apoptosis in the CNS may contribute to HIV neuropathogenesis.
  • Recruitment and infection of macrophages and microglia by apoptotic T lymphocytes could be a novel pathway for HIV spread.
  • This apoptosis-driven mechanism offers a new perspective on HIV's CNS involvement.

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