Laboratory of Preclinical Neurobiology, Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057, USA.
Cells. 2022 May 10;11(10):1599. doi: 10.3390/cells11101599.
Axonal degeneration and loss of synapses are often seen in different brain areas of people living with human immunodeficiency virus (HIV). Nevertheless, the underlying causes of the pathological alterations observed in these individuals are poorly comprehended, considering that HIV does not infect neurons. Experimental data have shown that viral proteins, including the envelope protein gp120, cause synaptic pathology followed by neuronal cell death. These neurotoxic effects on synapses could be the result of a variety of mechanisms that decrease synaptic plasticity. In this paper, we will briefly present new emerging concepts connected with the ability of gp120 to promote the degeneration of synapses by either directly damaging the axonal cytoskeleton and/or the indirect activation of the p75 neurotrophin receptor death domain in dendrites.
轴突变性和突触丧失在人类免疫缺陷病毒（HIV）感染者的不同大脑区域中经常出现。然而，考虑到 HIV 并不感染神经元，对于这些个体中观察到的病理改变的根本原因还了解甚少。实验数据表明，包括包膜蛋白 gp120 在内的病毒蛋白可导致突触病变，随后神经元细胞死亡。这些对突触的神经毒性作用可能是多种机制导致突触可塑性降低的结果。在本文中，我们将简要介绍与 gp120 促进突触退化的能力相关的新出现的概念，这些能力要么通过直接损害轴突细胞骨架，要么通过间接激活树突中的 p75 神经营养因子受体死亡结构域。
