       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).

