O'Connell Douglas, Liang Chengyu
a Department of Molecular Microbiology and Immunology , Keck Medical School, University of Southern California , Los Angeles , CA , USA.
Autophagy. 2016;12(3):451-9. doi: 10.1080/15548627.2016.1139262. Epub 2016 Mar 2.
More than 50% of the U.S. population is infected with herpes simplex virus type-I (HSV-1) and global infectious estimates are nearly 90%. HSV-1 is normally seen as a harmless virus but debilitating diseases can arise, including encephalitis and ocular diseases. HSV-1 is unique in that it can undermine host defenses and establish lifelong infection in neurons. Viral reactivation from latency may allow HSV-1 to lay siege to the brain (Herpes encephalitis). Recent advances maintain that HSV-1 proteins act to suppress and/or control the lysosome-dependent degradation pathway of macroautophagy (hereafter autophagy) and consequently, in neurons, may be coupled with the advancement of HSV-1-associated pathogenesis. Furthermore, increasing evidence suggests that HSV-1 infection may constitute a gradual risk factor for neurodegenerative disorders. The relationship between HSV-1 infection and autophagy manipulation combined with neuropathogenesis may be intimately intertwined demanding further investigation.
超过50%的美国人口感染了I型单纯疱疹病毒（HSV-1），全球感染率估计接近90%。HSV-1通常被视为一种无害病毒，但也可能引发使人衰弱的疾病，包括脑炎和眼部疾病。HSV-1的独特之处在于它能够破坏宿主防御并在神经元中建立终身感染。潜伏期的病毒再激活可能使HSV-1对大脑发起攻击（疱疹性脑炎）。最近的研究进展表明，HSV-1蛋白会抑制和/或控制巨自噬（以下简称自噬）的溶酶体依赖性降解途径，因此，在神经元中，这可能与HSV-1相关发病机制的进展有关。此外，越来越多的证据表明，HSV-1感染可能是神经退行性疾病的一个渐进性风险因素。HSV-1感染与自噬调控以及神经发病机制之间的关系可能紧密相连，需要进一步研究。
