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

TLDR

Viral infections can trigger or worsen autoimmune disease, possibly through viral antigens that mimic host proteins and activate self‑reactive T cells. In a murine model, an HSV‑1 coat protein epitope activated autoreactive T cells against corneal antigens, and viruses lacking this epitope failed to induce disease, demonstrating that viral molecular mimicry can drive post‑infection autoimmunity.

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.