Functional interaction and partial homology between human immunodeficiency virus and neuroleukin.
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.[1]References
- Functional interaction and partial homology between human immunodeficiency virus and neuroleukin. Lee, M.R., Ho, D.D., Gurney, M.E. Science (1987) [Pubmed]
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