Published online Jan 28, 2016. doi: 10.3748/wjg.v22.i4.1405
Peer-review started: June 4, 2015
First decision: September 11, 2015
Revised: November 17, 2015
Accepted: December 12, 2015
Article in press: December 14, 2015
Published online: January 28, 2016
Processing time: 236 Days and 0.9 Hours
Hepatitis C virus (HCV) is a hepato- and lymphotropic agent that is able to induce several autoimmune rheumatic disorders: vasculitis, sicca syndrome, arthralgias/arthritis and fibromyalgia. The severity of clinical manifestations is variable and sometimes life-threatening. HCV infection can mimic many primitive rheumatic diseases, therefore, it is mandatory to distinguish HCV-related manifestations from primitive ones because the prognosis and therapeutic strategies can be fairly dissimilar. The new direct-acting antivirals drugs can help to avoid the well-known risks of worsening or new onset of autoimmune diseases during the traditional interferon-based therapies.
Core tip: As a consequence of its lymphotropic nature, hepatitis C virus (HCV) can trigger and sustain a clonal B-cell expansion which causes a wide spectrum of autoimmune/lymphoproliferative disorders, through a multistep process. These extrahepatic manifestations become clinically manifest in 40%-70% of the patients and they can be frequently classified among the rheumatic ones. Furthermore, HCV can promote the production of several autoantibodies complicating the differential diagnosis between primitive and HCV-related rheumatic disorders.