Functional interaction and partial homology between human immunodeficiency virus and neuroleukin.
Functional interaction and partial homology between human immunodeficiency virus and neuroleukin.
复制标题
人类免疫缺陷病毒和神经白介素之间的功能相互作用和部分同源性。
DOI：
10.1126/science.3039662
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Gurney,ME
中科院分区：
文献类型：
--
作者：
Lee,MR;Ho,DD;Gurney,ME
痴呆症在艾滋病患者中很常见，但人类免疫缺陷病毒1型（HIV-1）导致神经损伤的机制尚不清楚。在这项研究中，HIV-1的抗原抑制神经元对神经营养因子的反应的可能性进行了检查。HIV-1和一种相关的逆转录病毒，猴免疫缺陷病毒（SIV），抑制鸡背根神经节的感觉神经元的生长，在培养基中含有神经白细胞介素（NLK），但在培养基中不含神经生长因子。一个无关的D型逆转录病毒，猴获得性免疫缺陷综合征病毒，不影响神经元的生长，在神经营养因子的存在。发现在NLK存在下HIV-1对神经元生长的抑制是由于gp 120包膜糖蛋白。gp 120和NLK之间的序列同源性区域可以解释gp 120的这种抑制特性，并且gp 120和NLK之间的功能相互作用在AIDS痴呆复合物的发病机制中可能是重要的。
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.