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Titolo:
HIV-1-induced neuronal injury in the developing brain
Autore:
Epstein, LG; Gelbard, HA;
Indirizzi:
Univ Rochester, Dept Neurol, Rochester, NY 14627 USA Univ Rochester Rochester NY USA 14627 ept Neurol, Rochester, NY 14627 USA Univ Rochester, Dept Pediat, Rochester, NY 14627 USA Univ Rochester Rochester NY USA 14627 ept Pediat, Rochester, NY 14627 USA Univ Rochester, Dept Microbiol, Rochester, NY 14627 USA Univ Rochester Rochester NY USA 14627 Microbiol, Rochester, NY 14627 USA Univ Rochester, Dept Immunol, Rochester, NY 14627 USA Univ Rochester Rochester NY USA 14627 pt Immunol, Rochester, NY 14627 USA Univ Rochester, Dept Pharmacol, Rochester, NY 14627 USA Univ Rochester Rochester NY USA 14627 Pharmacol, Rochester, NY 14627 USA
Titolo Testata:
JOURNAL OF LEUKOCYTE BIOLOGY
fascicolo: 4, volume: 65, anno: 1999,
pagine: 453 - 457
SICI:
0741-5400(199904)65:4<453:HNIITD>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; TUMOR-NECROSIS-FACTOR; PLATELET-ACTIVATING-FACTOR; CENTRAL-NERVOUS-SYSTEM; PRIMARY HUMAN ASTROCYTES; FACTOR-ALPHA; HIV-1 INFECTION; PROGRESSIVE ENCEPHALOPATHY; NEUROLOGIC MANIFESTATIONS; RECEPTOR ACTIVATION;
Keywords:
central nervous system; apoptosis; pathogenesis; blood-brain barrier; neuroprotection;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Epstein, LG Childrens Mem Hosp, 2300 Childrens Plaza 51, Chicago, IL 60614USA Childrens Mem Hosp 2300 Childrens Plaza 51 Chicago IL USA 60614
Citazione:
L.G. Epstein e H.A. Gelbard, "HIV-1-induced neuronal injury in the developing brain", J LEUK BIOL, 65(4), 1999, pp. 453-457

Abstract

HIV-1 infection of the nervous system causes neuronal injury and death, resulting in cognitive, motor, and behavioral dysfunction in both adults and children. in infants a characteristic feature of HIV-1 infection is impaired brain growth resulting in secondary microcephaly with onset between 2 and4 months of age. This post-natal period of brain development is particularly vulnerable to excitotoxic neuronal injury due to the active synaptogenesis and pruning that takes place at this age associated with over-expressionof excitatory amino acid (EAA) receptors, HIV-1 infection of brain microglia and perivascular macrophages results in chronic inflammation manifest pathologically as diffuse microglial activation and reactive astrogliosis. Several inflammatory products of activated microglia, including tumor necrosis factor alpha (TNF-alpha) and platelet-activating factor (PAF) have been shown to act as neuronal toxins. This toxic effect can be antagonized by blocking NMDA (or AMPA) glutamate receptors, suggesting that (weak) excitotoxicity leads to oxidative stress, neuronal injury, and apoptosis. HIV-1 infection and chronic inflammation may also contribute disruption of the blood-brain barrier and could result in further entry into the CNS of toxic viral or cellular products or additional HIV-l-infected cells, We hypothesize that prolonged microglial activation during HIV-1 infection underlies the neuronal injury and impaired brain growth in affected infants. Further investigation of the interaction between HIV-1-infected/activated microglia and developing neurons seems warranted. The current understanding of HIV neuropathogenesis implies that therapeutic strategies should target the sustained immune activation hi microglia, attempt to repair the integrity of the blood-brain barrier, and provide '"neuroprotection" from excitotoxic neuronal injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 18:14:58