Peterson P K, Chao C C, Molitor T, Murtaugh M, Strgar F, Sharp B M
Department of Medicine, Hennepin County Medical Center, Minnesota 55415.
Rev Infect Dis. 1991 Jul-Aug;13(4):710-20. doi: 10.1093/clinids/13.4.710.
Despite inherent difficulties in defining and measuring stress, a scientific framework has been provided in recent years for understanding how disruptive life experiences might be translated into altered susceptibility to infectious diseases. Studies of the effects of stress on pathogenesis of infectious disease are highly relevant to assessment of the biological importance of the immune impairments that have been associated with stress. With a few notable exceptions, investigations of viral infections in humans and in animal models support the hypothesis that stress promotes the pathogenesis of such infections. Similar conclusions can be drawn from studies of bacterial infections in humans and animals and from a small number of studies of parasitic infections in rodent models. While many of these studies have substantial limitations, the data nonetheless suggest that stress is a potential cofactor in the pathogenesis of infectious disease. Given recent unprecedented advances in the neurosciences, in immunology, and in the field of microbial pathogenesis, the relationship between stress and infection should be a fruitful topic for interdisciplinary research.
尽管在定义和测量压力方面存在内在困难，但近年来已提供了一个科学框架，用于理解破坏性的生活经历如何转化为对传染病易感性的改变。压力对传染病发病机制影响的研究与评估与压力相关的免疫损伤的生物学重要性高度相关。除了少数显著的例外情况，对人类和动物模型中病毒感染的研究支持了压力促进此类感染发病机制的假说。从对人类和动物细菌感染的研究以及对啮齿动物模型中寄生虫感染的少量研究中也可以得出类似的结论。虽然这些研究中有许多存在重大局限性，但数据仍然表明压力是传染病发病机制中的一个潜在辅助因素。鉴于神经科学、免疫学和微生物发病机制领域最近取得了前所未有的进展，压力与感染之间的关系应该是跨学科研究的一个富有成果的课题。
