Background: Myasthenia gravis (MG) is a chronic autoimmune disease affecting skeletal muscle characterized by autoantibodies distrupting normal signal transmission at neuromuscular junction; in most of cases antibodies are directed against acetylcholine receptor (AChR-Ab) and in a lower percentage of cases against muscle-specific tyrosine kinase (MuSK-Ab) or other antigens defining different disease subgroups. Mechanism of insurgence of MG has not been completely understood yet; recent evidences reported the development of MG after infection by West Nile virus (WNV), causative agent of neuroinvasive disease mainly transmitted with the bite of infected mosquitoes; moreover our previous results showed seropositivity for WNV antibodies in AChR-seropositive MG patients. A further analysis of patients affected by MG has been here conducted with the aim of expanding the screening for WNV-Ab to more patients and also subgrouping them on the basis of anti MuSK or anti AChR seropositivity.
Method and findings: We analyzed the serum from futher 10 MG patients seropositive for AChR-Ab and from 3 patients with MuSK-Ab but not AChR-Ab-seropositive, together with 20 control sera, for detection of WNV antibodies. Seropositivity for anti WNV IgG was obtained in 38% of MG patients, of which 23% were AChR-Ab positive and 15% were MuSK-Ab positive, although no previous WNV infection was reported. Control samples didn’t show seropositivity for anti WNV antibodies, except one who had ANCA-positive vasculitis and was also subjected to blood transfusion, a possible vehicle of WNV virus.
Discussion: Together with previously published data, total percentage of 23% seropositivity for WNV antibodies has been found in MG patients. It appears possible that viral antigen could break immunological self-tolerance by mechanisms of molecular mimicry between virus proteins and AChR subunits and/or MuSK and that this mechanism could be related to MG insurgence.
Marilena Greco, Pietro Cofano and Giambattista Lobreglio*
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