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Molecular Mimicry by Herpes Simplex Virus-Type 1: Autoimmune Disease After Viral Infection

1998; American Association for the Advancement of Science; Volume: 279; Issue: 5355 Linguagem: Inglês

10.1126/science.279.5355.1344

1095-9203

Zishan Zhao, Francesca Granucci, Lily Yeh, Priscilla A. Schaffer, Harvey Cantor,

Immunotherapy and Immune Responses

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.