Delery Elizabeth C, MacLean Andrew G
1 Tulane National Primate Research Center , Covington, Louisiana.
2 Tulane Program in Biomedical Sciences, Tulane Medical School , New Orleans, Louisiana.
Viral Immunol. 2019 Jan/Feb;32(1):55-62. doi: 10.1089/vim.2018.0093. Epub 2018 Sep 27.
Viral infection in the brain can be acute or chronic, with the responses often producing foci of increasingly cytotoxic inflammation. This can lead to effects beyond the central nervous system (CNS). To stimulate discussion, this commentary addresses four questions: What drives the development of human immunodeficiency virus (HIV)-associated neurocognitive disorders, does the phenotype of macrophages in the CNS spur development of HIV encephalitis (HIVE), does continual activation of astrocytes drive the development of HIV-associated neurocognitive disorders/subclinical disease, and neuroinflammation: friend or foe? A unifying theory that connects each question is the issue of continued activation of glial cells, even in the apparent absence of simian immunodeficiency virus/HIV in the CNS. As the CNS innate immune system is distinct from the rest of the body, it is likely there could be a number of activation profiles not observed elsewhere.
脑部的病毒感染可以是急性的或慢性的，其反应通常会产生细胞毒性越来越强的炎症病灶。这可能导致中枢神经系统（CNS）以外的影响。为了激发讨论，本评论探讨四个问题：是什么驱动了人类免疫缺陷病毒（HIV）相关神经认知障碍的发展，中枢神经系统中巨噬细胞的表型是否会促使HIV脑炎（HIVE）的发展，星形胶质细胞的持续激活是否会驱动HIV相关神经认知障碍/亚临床疾病的发展，以及神经炎症：是友还是敌？将每个问题联系起来的一个统一理论是神经胶质细胞持续激活的问题，即使在中枢神经系统中明显不存在猴免疫缺陷病毒/HIV的情况下也是如此。由于中枢神经系统的固有免疫系统与身体其他部位不同，很可能存在许多在其他地方未观察到的激活模式。
