Molecular Mimicry by Herpes Simplex Virus-Type 1: Autoimmune Disease After Viral Infection
Zi-Shan Zhao,
Francesca Granucci,
Lily Yeh,
Priscilla A. Schaffer,
*
Harvey Cantor
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.
Z.-S. Zhao, F. Granucci, H. Cantor, Department of Pathology,
Harvard Medical School, and Department of Cancer Immunology and AIDS,
Dana-Farber Cancer Institute, Boston, MA 02115, USA.
L. Yeh and P. A. Schaffer, Division of Molecular Genetics,
Dana-Farber Cancer Institute, Boston, MA 02115 USA.
*
Present address: Department of Microbiology, University of
Pennsylvania School of Medicine, Philadelphia, PA 19104 USA.
