Molecular mimicry is an immunological process whereby similar antigenic peptides induce cross-reactive immune responses in the body. It is a highly conserved phenomenon in nature that is found in most organisms, and can be used by pathogens to evade host defenses or even to hijack the host’s immune system.
Virus-induced molecular mimicry is one of the most studied forms of this process and it has been shown to occur in several models of infection, including hepatitis B virus (HBV) and lymphocytic choriomeningitis virus (LCMV) infections. This autoimmune response is thought to be caused by viral-induced microbial recognition of self epitopes on human cells and may result in tissue damage such as hepatitis or encephalomyelitis [10, 11, 13, 14].
Infectious diseases that utilize virus-induced molecular mimicry include adenoviruses, herpes simplex viruses, Epstein-Barr virus, hepatitis C virus, cytomegalovirus, and parvovirus B19. Moreover, several types of bacteria also use molecular mimicry to invade the host.
The role of a virus-induced molecular mimicry in autoimmune disease has been suggested for several disorders, including autoimmune hepatitis, multiple sclerosis, and lupus. A study using a natural infection model in SJL/J mice with the neurotropic picornavirus Theiler’s murine encephalomyelitis virus (TMEV) demonstrated that a 30-mer peptide from the immunodominant encephalitogenic myelin proteolipid protein (PLP139-151) induced CD4+ T cells to attack the myelin sheath. This inflammatory process subsequently led to progressive demyelination of the myelin sheath and neurological symptoms such as blindness and limb amputations.
Other microbial infections that have been reported to induce autoimmune disease by molecular mimicry are brucellosis, tuberculosis, and cholera. This is because the microbial proteins that trigger autoimmune diseases are often derived from pathogenic bacteria or viruses, and thus they share similar antigens with the underlying disease.
Immune cell recruitment and stimulation by molecular mimicry has been documented in other diseases such as rheumatoid arthritis, Behcet’s disease, and nephrotic syndrome. However, the exact mechanism of how this occurs remains a mystery, as it requires a prolonged period of latency between infection and development of the autoimmune condition.
In addition, the underlying immune mechanisms are not well understood, as they are complicated by numerous factors, such as the presence of non-specific immunity and heterologous immunity. The most important challenge for future studies is to develop a more detailed understanding of these complex processes. This can be achieved by applying new technologies in a more controlled manner, and also by further exploring the effects of molecular mimicry on specific immune cells or innate immunity.
