Key result
Viral infections promote autoimmunity mainly via nonspecific inflammation in susceptible hosts rather than molecular mimicry.
This review challenges the popular molecular mimicry hypothesis, proposing instead that viral-induced nonspecific inflammation is the primary trigger for autoimmunity in susceptible individuals.
May redirect mechanistic focus from molecular mimicry to nonspecific inflammation in virus-triggered autoimmunity; hypothesis-generating for prospective validation in susceptible hosts.
Viruses are considered as causative agents and contributors to lesion expression in autoimmune disease, notions best supported by studies in animal model systems. This review discusses relationships between virus infection and autoimmunity focusing on mechanisms by which they could induce autoreactivity. The popular idea of molecular mimicry is viewed skeptically with the reviewers taking the viewpoint that viruses contribute to autoimmunity mainly by inducing several nonspecific inflammatory events that together are sufficient to trigger autoreactivity in genetically receptive hosts.
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Rouse et al. (2002) conducted a review in Autoimmune disease. Virus infection was evaluated. Virus infection contributes to autoimmunity mainly by inducing nonspecific inflammatory events that trigger autoreactivity in genetically receptive hosts, rather than through molecular mimicry.
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