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J Biol Chem, Vol. 273, Issue 28, 17852-17858, July 10, 1998
From the Departments of a Neurobiology and Anatomy,
b Dental Research, d Neurology (Child Neurology
Division), e Pediatrics, c Microbiology and Immunology,
i Pharmacology and Physiology, and the g Cancer Center,
University of Rochester Medical Center,
Rochester, New York, 14642
Human immunodeficiency virus type 1 (HIV-1)
infection of the central nervous system may result in neuronal
apoptosis in vulnerable brain regions, including cerebral cortex and
basal ganglia. The mechanisms for neuronal loss are likely to be
multifactorial and indirect, since HIV-1 productively infects
brain-resident macrophages and microglia but does not cause cytolytic
infection of neurons in the central nervous system. HIV-1 infection of
macrophages and microglia leads to production and release of diffusible
factors that result in neuronal cell death, including the HIV-1
regulatory protein Tat. We demonstrate in this report that recombinant
Tat1-86 and Tat peptides containing the basic region
induce neuronal apoptosis in approximately 50% of vulnerable neurons
in both rat and human neuronal cultures, and this apoptotic cell death
is mediated by release of the pro-inflammatory cytokine tumor necrosis
factor
HIV-1 Tat Induces Neuronal Death via Tumor Necrosis Factor-
and Activation of Non-N-methyl-D-aspartate
Receptors by a NF
B-Independent Mechanism
, and by activation of glutamate receptors of the
non-N-methyl-D-aspartate subtype. Finally, we
show that Tat-induced apoptosis of human neuronal cell cultures occurs
in the absence of activation of the transcription factor NF
B. These
findings further define cellular pathways activated by Tat, that
dysregulate production of tumor necrosis factor , and lead to
activation of glutamate receptors and neuronal death during HIV-1
infection of the central nervous system.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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