Langford Dianne, Masliah Eliezer
Department of Pathology, University of California, San Diego, La Jolla, California, USA.
J Neurovirol. 2002 Dec;8(6):625-38. doi: 10.1080/13550280290100996.
Viral infection of the central nervous system elicits a myriad of cellular, vascular, and neuroimmune factors that contribute to acute, subacute, and chronic damage to the brain. In response to cellular damage, the host is capable of producing trophic factors that may protect neuronal, glial, and endothelial cell populations. Both neurotrophic and angiotrophic factors can also operate by modulating the neuroimmune response, which plays a central role in the pathogenesis of the neurodegenerative process. In this regard, crosstalk signaling among host cells, components of the neuroimmune response, and virus could influence cell fate by production of trophic factors that protect or rescue neurons vulnerable to viral damage. In this context, the main objective of this review is to provide an overview of evidence in support of the role of trophic factors in regulating the neuroimmune response in chronic viral infections of the central nervous system. Special emphasis is placed on the interaction of the human immunodeficiency virus (HIV) Tat protein with endothelial, astroglial, microglial, and neuronal cells, resulting in altered expression of vascular endothelial growth factor, fibroblast growth factor, interleukin-8, and regulation of calcium flux via CXCR2, which directly influences neuronal cell fitness.
中枢神经系统的病毒感染会引发众多细胞、血管和神经免疫因子，这些因子会导致大脑出现急性、亚急性和慢性损伤。作为对细胞损伤的反应，宿主能够产生可能保护神经元、神经胶质细胞和内皮细胞群体的营养因子。神经营养因子和血管营养因子也可以通过调节神经免疫反应发挥作用，而神经免疫反应在神经退行性过程的发病机制中起着核心作用。在这方面，宿主细胞、神经免疫反应成分和病毒之间的串扰信号传导可能通过产生保护或拯救易受病毒损伤的神经元的营养因子来影响细胞命运。在此背景下，本综述的主要目的是概述支持营养因子在调节中枢神经系统慢性病毒感染中的神经免疫反应方面作用的证据。特别强调人类免疫缺陷病毒（HIV）Tat蛋白与内皮细胞、星形胶质细胞、小胶质细胞和神经元细胞的相互作用，这会导致血管内皮生长因子、成纤维细胞生长因子、白细胞介素-8的表达改变，以及通过CXCR2调节钙通量，而这直接影响神经元细胞的健康状况。
