Molecular mimicry, viruses

Olson, J.K. et al., A virus-induced molecular mimicry model of multiple sclerosis, J. Clin. 

There is considerable interest in the role of infectious agents in the development of autoimmune diseases. Some of this interest is based on the concept of molecular mimicry as a causal mechanism. Molecular mimicry refers to the possible pathologic role of cross-reactive antibodies or T cells to a self-antigen that is structurally similar to, and thus shares epitopes with, a viral or other infectious agent. For most autoimmune diseases, however, evidence of molecular mimicry leading to disease is not conclusive.1819 Viruses and other infections also have a less-specific immune effect, stimulating toll-like receptors and proinflammatory cytokine secretion, which is another mechanism that has been postulated to influence autoimmune disease risk.20... 

Antigens with molecular mimicry. There is also evidence that antibodies induced by viruses or bacteria can cross-react with autoantigens. 

Bystander activation activation of autoreactive cells through nonspecific inflammation and induction of inflammatory cytokines and chemokines is also of pathological consequence in MS. It has been suggested that bystander activation, induced by persistent virus infection or primed by molecular mimicry may activate autoreactive T-cells specific for the CNS (McCoy et al., 2006). Einally, cryptic antigens may also play a role in immune activation. In other immune-mediated diseases such as Chronic Lymphocytic Thyroiditis and Chagas Heart Disease, exposure of cryptic epitopes leads to the activation of autoimmune cells and further contributes to... 

McCoy L, Tsunoda I, Fujinami RS (2006) Muldple sclerosis and virus induced immune responses Autoimmunity can be primed by molecular mimicry and augmented by bystander aedvadon. Autoimmunity 39 9—19. 

Levin MC, Lee SM, Morcos Y, Brady J, Stuar t J (2002a) Crossreactivity between immuiiodominant human T lymphoti opic virus type I tax and neui ons Implicadons for molecular mimicry. J hifectDis 186 1514-1517. 

Various viruses encode proteins with sequenee homology to host proteins which are known to be involved in host defense functions. Viruses pirate and modify key immunoregulatory molecules, by use of molecular mimicry, to elude the Immune system (Murphy, 1997). Viruses also encode proteins that exploit or alter their host cells, replicate or induce migration for virus dissemination. Interestingly, DNA viruses such as the Herpesviruses (Cytomegalovirus (CMV), human herpesvirus (HHV-6 and 7), herpesvirus Saimiri (HVS) and Kaposi s sarcoma-associated Herpesvirus (KSHV)) all express GPCRs (Table 2). 

TlDM was previously known as insulin-dependent diabetes meUi-tus (IDDM) and juvenile-onset diabetes (JOD). It occurs in 0.5% of the population, and is characterised by sudden onset, usually before 25 years of age, and weight loss. The -cells are destroyed by autoimmune attack following viral infection. Molecular mimicry is thought to be the cause. This happens when parts of a virus protein resembie a protein in the host s P-cells. The body s immune defences then attack both the virus and the P-cells, which are destroyed hence insulin secretion ceases causing TIDM. 

The term molecular mimicry (34), is difficult to define, in part, because it does not represent a single concept (35,36). In this review, we use the term in the sense of adaptive molecular mimicry as proposed by Roger Hall in 1994 (37). According to Hall, adaptive molecular mimicry means that a parasite (bacteria, fungi, virus, helminth, protozoa) molecule mimics a host molecule for a biological reason, and the homologous functional structure resides in a parasite molecule which is otherwise dissimilar to... 

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