Rheumatologic complications of hepatitis C virus (HCV) infection are common and include mixed cryoglobulinemia, vasculitis, sicca symptoms, myalgia, arthritis, and fibromyalgia. The prevalence of cryoglobulinemia in Sweden and Germany is much lower compared with data from southern Europe. Viral, genetic, or environmental factors may be responsible for such a difference in prevalence. There is no single clinical picture of arthritis in patients with HCV infection. There is a well-defined picture of arthritis associated with the presence of mixed cryoglobulinemia that consists of an intermittent mono- or oligoarticular, nondestructive arthritis affecting large and medium-size joints. Involvement of salivary and lacrimal glands is common in HCV-infected subjects, but HCV antigens are not detected in affected glands. HCV-infected subjects express a high prevalence of a variety of autoantibodies, usually in low titers. The clinical significance of most of these autoantibodies is not clear. The prevalence and titer of these autoantibodies are unaffected by interferon-alpha therapy. Several studies have attempted to assess whether HCV infection may be involved in the etiopathogenesis of rheumatic and autoimmune diseases. The results of most of these studies do not support the idea that HCV infection may play a pathogenic role in the development of systemic lupus erythematosus, antiphospholipid syndrome, or leukocytoclastic vasculitis. Experience treating patients with HCV-associated arthritis is limited and treatment remains controversial. No major therapeutic trials in HCV-associated arthritis were reported in the past 2 years.