home
***
CD-ROM
|
disk
|
FTP
|
other
***
search
/
Shareware Overload Trio 2
/
Shareware Overload Trio Volume 2 (Chestnut CD-ROM).ISO
/
dir26
/
med9409d.zip
/
M9490524.TXT
< prev
next >
Wrap
Text File
|
1994-09-24
|
3KB
|
42 lines
Document 0524
DOCN M9490524
TI HIV-1 infection of the developing nervous system: central role of
astrocytes in pathogenesis.
DT 9411
AU Blumberg BM; Gelbard HA; Epstein LG; Department of Neurology, University
of Rochester, NY 14642.
SO Virus Res. 1994 May;32(2):253-67. Unique Identifier : AIDSLINE
MED/94346056
AB Recent studies in our laboratory and that of Dr. Howard Gendelman have
revealed two important pathways for neuronal damage during HIV-1
encephalopathy in children. First, substantial numbers of astrocytes are
actively or latently infected with HIV-1. Astrocyte infection may lead
to neuronal dysfunction through loss of supporting growth factors,
excitotoxicity due to dysregulation of neurotransmitter reuptake, and
loosening of the blood-brain barrier permitting further seeding of HIV-1
in the CNS. Significantly, infection of astrocytes is marked by
near-exclusive synthesis of early regulatory gene products of HIV-1,
while structural proteins characteristic of productive infection are
found in macrophages, microglia and multinucleated giant cells. We
propose the term 'restricted' to denote the non-productive infection
found in astrocytes. Second, HIV-1-infected macrophages initiate
inflammatory processes which are amplified through cell-cell
interactions with astrocytes. Macrophage-astrocyte interactions produce
arachidonic metabolites and potentially neurotoxic cytokines (TNF-alpha
and IL-1 beta), leading to astroglial activation and proliferation which
then amplifies these cellular processes. These new findings suggest that
two major pathways leading to neurotoxicity in pediatric AIDS
encephalopathy are linked to HIV-1 infection through astrocyte-mediated
processes, and help explain how small numbers of productivity infected
cells indirectly cause widespread tissue pathology and elicit profound
neurological impairment.
DE Astrocytes/MICROBIOLOGY/PATHOLOGY/*PHYSIOLOGY AIDS Dementia
Complex/*ETIOLOGY/MICROBIOLOGY/PATHOLOGY Cell Communication Cell Death
Child Human *HIV-1/PHYSIOLOGY/PATHOGENICITY
Macrophages/MICROBIOLOGY/PHYSIOLOGY Support, Non-U.S. Gov't Support,
U.S. Gov't, P.H.S. JOURNAL ARTICLE REVIEW REVIEW, ACADEMIC
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).