Key result
Virus infections are implicated in the initiation, progression, and perpetuation of autoimmune diseases through mechanisms including molecular mimicry, epitope spreading, and bystander activation.
This review summarizes the mechanisms by which viral infections may initiate, perpetuate, and progress T-cell-mediated autoimmune diseases.
Viral triggers may warrant consideration in autoimmune evaluation; leaves open whether antivirals alter disease course.
Virus infections have been implicated in the initiation of multiple human autoimmune diseases. This article focuses on reviewing the role of viruses in initiation, progression, and perpetuation of autoimmune diseases. Various mechanisms by which virus infections can induce autoimmune responses including molecular mimicry, epitope spreading, direct bystander activation, and release of cryptic epitopes are discussed. Evidence implicating virus infections in the pathogenesis of various human autoimmune diseases is reviewed. Last, the characteristics of animal models that have been developed for the study of the potential role of viruses in the initiation and progression of autoimmune disease are reviewed.
No takes yet. Share an insight, caveat, or question.
Olson et al. (2001) conducted a review in Autoimmune diseases. Virus infections was evaluated. Virus infections are implicated in the initiation, progression, and perpetuation of autoimmune diseases through mechanisms including molecular mimicry, epitope spreading, and bystander activation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: