Institute of Endocrinology and Diabetes, The Children's Hospital at Westmead, Sydney, NSW, Australia.
Autoimmun Rev. 2014 Jun;13(6):635-40. doi: 10.1016/j.autrev.2013.12.003. Epub 2014 Jan 11.
An autoimmune disease (AD), organ-specific or systemic, results from an aberrant response in which the protective immune system normally schooled to recognize and destroy invading infectious agents (viruses, etc.) instead fails to distinguish self-antigens and proceeds to attack and destroy the host's organs. There can be familial aggregation in which a single AD may occur in members of a family, or a single family may be afflicted with multiple ADs. Finally, sometimes multiple ADs co-occur in a single individual: the kaleidoscope of autoimmunity. Autoimmunity is a multifactorial process in which genetic, hormonal, immunological and environmental factors act in concert to materialize the mosaic of autoimmunity phenomenon. A genetically primed individual may yet not develop an AD: the contribution by an environmental factor (non-infectious or infectious) is essential for completion of the act. Of the non-infectious factors, stress plays a determinative step in autoimmunity in that it abrogates viral latency and thereby ordains the viruses to qualify as infectious environmental factors that trigger ADs. This is note-worthy as viruses rank first as the most important environmental triggers of ADs. Furthermore, all these viruses experience going through latency. Hence the hypothesis: "The abrogation of viral latency by stress, a non-infectious environmental agent, is an intrinsic prerequisite prelude before viruses can rank as infectious environmental agents that trigger autoimmune diseases". There is collaboration here between non-infectious- and infectious-agent to achieve the cause of autoimmunity. We say viral latency and stress have a covenant: continued perpetration of autoimmunity is dependent on the intervention by stress to reactivate latent infections.
自身免疫性疾病（AD）是一种器官特异性或全身性疾病，是由于保护免疫系统异常反应引起的，正常情况下，免疫系统能够识别和摧毁入侵的传染性病原体（病毒等），但在自身免疫性疾病中，免疫系统无法区分自身抗原，进而攻击和破坏宿主的器官。在某些情况下，单一的 AD 可能会在家族成员中出现，即家族聚集性 AD，或者一个家族可能会受到多种 AD 的影响。最后，有时单一个体中会同时出现多种 AD，即自身免疫的万花筒现象。自身免疫是一个多因素过程，遗传、激素、免疫和环境因素协同作用，共同导致自身免疫现象的马赛克出现。具有遗传倾向的个体可能仍不会发展为 AD：环境因素（非传染性或传染性）的贡献对于完成这一过程至关重要。在非传染性因素中，压力在自身免疫中起着决定性的作用，因为它会破坏病毒潜伏期，从而使病毒成为触发 AD 的传染性环境因素。这一点值得注意，因为病毒是 AD 最重要的环境触发因素之一。此外，所有这些病毒都经历潜伏期。因此，我们提出了这样一个假设：“压力（一种非传染性环境因素）破坏病毒潜伏期，是病毒成为触发自身免疫性疾病的传染性环境因素的内在先决条件”。非传染性和传染性因素在这里协同作用，导致自身免疫的发生。我们说病毒潜伏期和压力之间存在着一种约定：持续的自身免疫依赖于压力的干预来重新激活潜伏感染。
