is triggered by exogenous antigen that progresses to a truly autoimmune response against mimicked self antigen and other antigens. from these examples, it is clear that the search for candidate mimic epitopes must extend beyond the immunodominant epitopes of a given autoimmune response. implications in human disease diseases of the central nervous system the hiv-1 virus has been shown to cause diseases of the central nervous system (cns) in humans through a molecular mimicry apparatus. hiv-1 gp41 is used to bind chemokines on the cell surface of the host so that the virion may gain entrance into the host. astrocytes are cells of the cns which are used to regulate the concentrations of k+ and neurotransmitter which enter the cerebrospinal fluid (csf) to contribute to the blood brain barrier. a twelve amino acid sequence (leu-gly-ile-trp-gly-cys-ser-gly-lys-leu-ile-cys) on gp41 of the hiv-1 virus (immunodominant region) shows sequence homology with a twelve amino acid protein on the surface of human astrocytes. antibodies are produced for the hiv-1 gp41 protein. these antibodies can cross-react with astrocytes within human cns tissue and act as autoantibodies. this contributes to many cns complications found in aids patients. theiler's murine encephalomyelitis virus (tmev) leads to the development in mice of a progressive cd4+ t cell-mediated response after these cells have infiltrated the cns. this virus has been shown to cause cns disease in mice that resembles multiple sclerosis, an autoimmune disease in humans that results in the gradual destruction of the myelin sheath coating axons of the cns. the tmev mouse virus shares a thirteen amino acid sequence (his-cys-leu-gly-lys-trp-leu-gly-his-pro-asp-lys-phe) (plp (proteolipid protein) 139-151 epitope) with that of a human myelin-specific epitope. bystander myelin damage is caused by virus specific th1 cells that cross react with this self epitope. to test the efficacy in which tmev uses molecular mimicry to its advantage, a sequence of the human myelin-specific epitope was inserted into a non-pathogenic tmev variant. as a result, there was a cd4+ t cell response and autoimmune demyelination was initiated by infection with a tmev peptide ligand. in humans, it has recently been shown that there are other possible targets for molecular mimicry in patients with multiple sclerosis. these involve the hepatitis b virus mimicking the human proteolipid protein (myelin protein) and the epstein-barr virus mimicking anti-myelin oligodendrocyte glycoprotein (contributes to a ring of myelin around blood vessels) or the glial cell adhesion protein (glialcam) found in the cns. muscle disorders myasthenia gravis is another common autoimmune disease. this disease causes fluctuating muscle weakness and fatigue. the disease occurs due to detectable antibodies produced against the human acetylcholine receptor. the receptor contains a seven amino acid sequence (trp-thr-tyr-asp-gly-thr-lys) in the α-subunit that demonstrates immunological cross-reactivity with a shared immunodominant domain of gpd of the herpes simplex virus (hsv). similar to hiv-1, gpd also aids in binding to chemokines on the cell surface of the host to gain entry into the host. cross-reactivity of the self epitope (α-subunit of the receptor) with antibodies produced against hsv suggests that the virus is associated with the initiation of myasthenia gravis. not only does hsv cause immunologic cross-reactivity, but the gpd peptide also competitively inhibits the binding of antibody made against the α-subunit to its corresponding peptide on the α-subunit. despite this, an autoimmune response still occurs. this further shows an immunologically significant sequence homology to the biologically active site of the human acetylcholine receptor. control there are ways in which autoimmunity caused by molecular mimicry can be avoided. control of the initiating factor (pathogen) via vaccination seems to be the most common method to avoid autoimmunity. inducing tolerance to the host autoantigen in this way may also be the most stable factor. the development of a downregulating immune response to the shared epitope between pathogen and host may be the best way of treating an autoimmune disease caused by molecular mimicry. alternatively, treatment with immunosuppressive drugs such as ciclosporin and azathioprine has also been used as a possible solution. however, in many cases this has been shown to be ineffective because cells and tissues have already been destroyed at the onset of the infection. conclusion the concept of molecular mimicry is a useful tool in understanding the etiology, pathogenesis, treatment, and prevention of autoimmune disorders. molecular mimicry is, however, only one mechanism by which an autoimmune disease can occur in association with a pathogen. understanding the mechanisms of molecular mimicry may allow future research to be directed toward uncovering the initiating infectious agent as well as recognizing the self determinant. this way, future research may be able to design strategies for treatment and prevention of autoimmune disorders. the use of transgenic models such as those used for discovery of the mimicry events leading to diseases of the cns and muscle disorders has helped evaluate the sequence of events leading to molecular mimicry. related terms viral apoptotic mimicry, defined by the exposure of phosphatidylserine (a marker for apoptosis) on the pathogen surface – in the case of apoptosis, the dead cell surface that is used to gain viral access to the interior of immune cells.