Isolation, Characterization, and Molecular Modeling of a Rheumatoid Factor from a Hepatitis C Virus Infected Patient with Sjögren's Syndrome

Lee, Yu-Ching; Tsai, Keng-Chang; Leu, Sy-Jye; Wang, Tuan-Jen; Liu, Chia-Yu; Yang, Yi-Yuan

Sjögren's syndrome (SS) is an autoimmune disorder that mainly affects the exocrine glands and usually presents as persistent dryness of the mouth and eyes due to functional impairment of the salivary and lachrymal glands [1] . SS occurs in a primary form not associated with other diseases and in a secondary form that complicates other rheumatic conditions, with the most common being rheumatoid arthritis. Positive RF was found in 96% of the patients with main extraglandular SS [2] . On the other hand, circulating monoclonal immunoglobulins (IgM kappa or IgG lambda) were detected in a significant higher frequency (43%) of SS-HCV patients as compared with the primary SS patients [3] . 2 The Scientific World Journal Hepatitis C virus (HCV) has been demonstrated to be one of the most likely candidates as a potential pathogenic agent causing SS in a subset of patients [2, 4, 5] . Many rheumatologic manifestations associated with chronic HCV infection include arthralgia, myalgia, arthritis, vasculitis, and sicca syndrome [6] . Clinical studies suggest the possibility of a close relationship among SS, HCV, and B-cell lymphoproliferative disorders [2, 4] . This triple association suggests an important role of associated autoimmune and/or chronic viral diseases in the pathogenesis of B-cell lymphoproliferative disorders and reinforces the hypothesis of a link among autoimmunity, infection, and cancer [4] .