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

Science. 1998 Feb 27;279(5355):1344-7. doi: 10.1126/science.279.5355.1344.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adoptive Transfer
  • Amino Acid Sequence
  • Animals
  • Autoantigens / immunology
  • Autoimmune Diseases / immunology*
  • CD4-Positive T-Lymphocytes / immunology
  • Capsid / chemistry
  • Capsid / genetics
  • Capsid / immunology*
  • Capsid Proteins*
  • Cornea / immunology*
  • Epitopes
  • Eye Proteins / immunology
  • Herpesvirus 1, Human / immunology*
  • Keratitis, Herpetic / immunology*
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Mice, SCID
  • Molecular Mimicry*
  • Molecular Sequence Data
  • Mutagenesis, Site-Directed
  • Oligopeptides / immunology
  • Viral Proteins

Substances

  • Autoantigens
  • Capsid Proteins
  • Epitopes
  • Eye Proteins
  • Oligopeptides
  • Viral Proteins
  • DNA cleavage and packaging proteins, Herpesvirus