Valyi-Nagy T, Dermody T S
Department of Pathology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.
Histol Histopathol. 2005 Jul;20(3):957-67. doi: 10.14670/HH-20.957.
Oxidative stress, primarily due to increased generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), is a feature of many viral infections. ROS and RNS modulate the permissiveness of cells to viral replication, regulate host inflammatory and immune responses, and cause oxidative damage to both host tissue and progeny virus. The lipid-rich nervous system is particularly susceptible to lipid peroxidation, an autocatalytic process that damages lipid-containing structures and yields reactive by-products, which can covalently modify and damage cellular macromolecules. Oxidative injury is a component of acute encephalitis caused by herpes simplex virus type 1 and reovirus, neurodegenerative disease caused by human immunodeficiency virus and murine leukemia virus, and subacute sclerosing panencephalitis caused by measles virus. The extent to which oxidative damage plays a beneficial role for the host by limiting viral replication is largely unknown. An enhanced understanding of the role of oxidative damage in viral infections of the nervous system may lead to therapeutic strategies to reduce tissue damage during viral infection without impeding the host antiviral response.
氧化应激主要是由于活性氧（ROS）和活性氮（RNS）生成增加所致，是许多病毒感染的一个特征。ROS和RNS调节细胞对病毒复制的易感性，调节宿主的炎症和免疫反应，并对宿主组织和子代病毒造成氧化损伤。富含脂质的神经系统特别容易受到脂质过氧化的影响，脂质过氧化是一个自催化过程，会损害含脂质的结构并产生反应性副产物，这些副产物可共价修饰并损害细胞大分子。氧化损伤是由1型单纯疱疹病毒和呼肠孤病毒引起的急性脑炎、由人类免疫缺陷病毒和鼠白血病病毒引起的神经退行性疾病以及由麻疹病毒引起的亚急性硬化性全脑炎的一个组成部分。氧化损伤通过限制病毒复制对宿主发挥有益作用的程度在很大程度上尚不清楚。深入了解氧化损伤在神经系统病毒感染中的作用可能会带来治疗策略，以减少病毒感染期间的组织损伤，同时不妨碍宿主的抗病毒反应。
