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1996-02-26
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Document 0295
DOCN M9620295
TI Apoptosis and HIV neuropathogenesis.
DT 9602
AU Espey MG; Biology Department, Georgetown University, Washington, DC
20057,; USA.
SO Med Hypotheses. 1995 Jun;44(6):536-8. Unique Identifier : AIDSLINE
MED/96038381
AB A consequence of HIV infection may be neurological dysfunction secondary
to the presence of virus in the central nervous system (CNS). The CNS
tropism of HIV and the mechanisms that govern its dissemination are not
well defined. One view is that HIV enters the brain through the
diapedesis of infected monocytes from blood into the perivascular space.
HIV may then spread to susceptible cells throughout parenchyma. An
alternate hypothesis is presented, which suggests that T lymphocyte
apoptosis may also participate in HIV entry and dissemination in the
brain. This is based on the following observations: 1) T lymphocyte
apoptosis may be a CNS-specific mechanisms to control inflammation, 2)
the most common circulating reservoir of HIV is the T lymphocyte, 3)
uninfected macrophages recruited to phagocytize HIV infected apoptotic T
lymphocytes in vitro can become productively infected, and 4) the
predominant form of HIV in the CNS is unintegrated. Aberrantly high
levels of apoptosis in HIV infected lymphocytes within the CNS and
subsequent recruitment and infection of macrophages and microglia may be
a novel component of HIV neuropathogenesis.
DE *Apoptosis AIDS Dementia Complex/IMMUNOLOGY/*PHYSIOPATHOLOGY Central
Nervous System/*PHYSIOPATHOLOGY/VIROLOGY Human *HIV/ISOLATION & PURIF
HIV Infections/IMMUNOLOGY/PHYSIOPATHOLOGY
T-Lymphocytes/IMMUNOLOGY/PHYSIOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).