Libbey Jane E, Fujinami Robert S
Department of Neurology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Clin Microbiol Newsl. 2002 May 15;24(10):73-76. doi: 10.1016/S0196-4399(02)80019-8. Epub 2002 Jul 25.
Viruses have been implicated in the initiation, progression, and exacerbation of several human autoimmune diseases, including multiple sclerosis. However, no single virus has been demonstrated as the etiologic agent. Multiple different infections may be involved, first in priming the immune system for autoimmunity and then in triggering the actual disease. A model based on experimental allergic encephalomyelitis, an animal model of multiple sclerosis, has been developed, which shows that an initial early infection with a virus having molecular mimicry to self-epitopes can prime for disease that occurs after a subsequent non-specific immunologic stimulus, such as a different infection. The role of multiple infections in the development of autoimmune disease may explain why no one virus has been implicated.
病毒已被认为与包括多发性硬化症在内的多种人类自身免疫性疾病的起始、进展和恶化有关。然而，尚无单一病毒被证实为病原体。可能涉及多种不同的感染，首先是使免疫系统对自身免疫产生致敏，然后引发实际疾病。基于实验性变应性脑脊髓炎（一种多发性硬化症的动物模型）开发了一个模型，该模型表明，最初早期感染一种与自身表位具有分子模拟的病毒，可使机体对随后的非特异性免疫刺激（如不同感染）引发的疾病产生致敏。多种感染在自身免疫性疾病发展中的作用可能解释了为何尚无单一病毒被牵连其中。
