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Science 28 August 1987:
Vol. 237. no. 4818, pp. 1047 - 1051
DOI: 10.1126/science.3039662

Articles

Science, Vol 237, Issue 4818, 1047-1051
Copyright © 1987 by American Association for the Advancement of Science


articles

Functional interaction and partial homology between human immunodeficiency virus and neuroleukin

MR Lee, DD Ho, and ME Gurney

Dementia is common in patients with AIDS, but the mechanism by which the human immunodeficiency virus type 1 (HIV-1) causes the neurological impairment is unknown. In this study the possibility that an antigen of HIV-1 suppresses neuronal responses to neurotrophic factors was examined. Both HIV-1 and a related retrovirus, simian immunodeficiency virus (SIV), inhibited the growth of sensory neurons from chick dorsal root ganglia in medium containing neuroleukin (NLK) but not in medium containing nerve growth factor. An unrelated type D retrovirus, simian acquired immunodeficiency syndrome virus, did not affect the growth of neurons in the presence of either neurotrophic factor. The inhibition by HIV-1 of neuron growth in the presence of NLK was found to be due to the gp120 envelope glycoprotein. Regions of sequence homology between gp120 and NLK may account for this inhibitory property of gp120 and functional interactions between gp120 and NLK may be important in the pathogenesis of the AIDS dementia complex.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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Growth Factors for Neuronal Survival and Process Regeneration: Implications in the Mammalian Central Nervous System.
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The Acquired Immunodeficiency Syndrome (AIDS) Dementia Complex.
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Ann Intern Med 111, 400-410
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Second conserved domain of gp120 is important for HIV infectivity and antibody neutralization.
D. Ho, J. Kaplan, I. Rackauskas, and M. Gurney (1988)
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The brain in AIDS: central nervous system HIV-1 infection and AIDS dementia complex.
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