mimicry by HSV-1 (KOS) is essential for
disease induction in genetically susceptible
hosts under all circumstances. Mimicry
mechanisms may be particularly important
in translating relatively low level viral in-
fections into an autoimmune response. In-
fections by higher concentrations of HSV-1
(KOS) or by more virulent strains of HSV-1
may induce inflammatory responses that are
sufficient to provoke autoimmune disease
without the need for molecular mimicry. A
comparison of HSK in transgenic mice with
T cells that carry a receptor specific for an
HSV-1 (KOS) viral peptide mimic or an
unrelated peptide should further clarify the
relative roles of mimicry and inflammation
in the pathogenesis of virally induced auto-
immune disease.
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