Molecular mimicry by herpes simplex virus-type 1: autoimmune disease after viral infection

ZS Zhao, F Granucci, L Yeh, PA Schaffer, H Cantor - Science, 1998 - science.org
ZS Zhao, F Granucci, L Yeh, PA Schaffer, H Cantor
Science, 1998science.org
Viral infection is sometimes associated with the initiation or exacerbation of autoimmune
disease, although the underlying mechanisms remain unclear. One proposed mechanism is
that viral determinants that mimic host antigens trigger self-reactive T cell clones to destroy
host tissue. An epitope expressed by a coat protein of herpes simplex virus–type 1 (HSV-1)
KOS strain has now been shown to be recognized by autoreactive T cells that target corneal
antigens in a murine model of autoimmune herpes stromal keratitis. Mutant HSV-1 viruses …
Viral infection is sometimes associated with the initiation or exacerbation of autoimmune disease, although the underlying mechanisms remain unclear. One proposed mechanism is that viral determinants that mimic host antigens trigger self-reactive T cell clones to destroy host tissue. An epitope expressed by a coat protein of herpes simplex virus–type 1 (HSV-1) KOS strain has now been shown to be recognized by autoreactive T cells that target corneal antigens in a murine model of autoimmune herpes stromal keratitis. Mutant HSV-1 viruses that lacked this epitope did not induce autoimmune disease. Thus, expression of molecular mimics can influence the development of autoimmune disease after viral infection.
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