Department of Ophthalmology, China-Japan Union Hospital of Jilin University, Changchun, China.
Department of Ophthalmology, Jilin City Central Hospital, Jilin, China.
Front Immunol. 2020 May 13;11:766. doi: 10.3389/fimmu.2020.00766. eCollection 2020.
Herpes stromal keratitis (HSK) is one of the primary diseases that cause vision loss or even blindness after herpes simplex virus (HSV)-1 infection. HSK-associated vision impairment is predominantly due to corneal scarring and neovascularization caused by inflammation. In the infected cornea, HSV can activate innate and adaptive immune responses of host cells, which triggers a cascade of reactions that leads to the release of inflammatory cytokines, chemokines, microRNA, and other regulatory factors that have stimulating or inhibitory effects on tissue. Physiologically, host cells show homeostasis. In this review, we summarize the factors involved in HSK pathogenesis from the perspective of immunity, molecules, and pathological angiogenesis. We also describe in detail the pathogenesis of chronic inflammatory lesions of the corneal stroma in response to HSV-1 infection.
单纯疱疹病毒性角膜炎（HSK）是单纯疱疹病毒（HSV）-1 感染后导致视力丧失甚至失明的主要疾病之一。HSK 相关的视力损害主要是由于炎症引起的角膜瘢痕和新生血管形成。在受感染的角膜中，HSV 可以激活宿主细胞的固有和适应性免疫反应，引发一系列反应，导致炎症细胞因子、趋化因子、microRNA 和其他对组织具有刺激或抑制作用的调节因子的释放。在生理上，宿主细胞表现出稳态。在这篇综述中，我们从免疫、分子和病理性血管生成的角度总结了 HSK 发病机制涉及的因素。我们还详细描述了宿主细胞对 HSV-1 感染的反应中角膜基质慢性炎症病变的发病机制。
