Arthralgia and/or arthritis are well-recognized and relatively common occurrences with viral infections. This topic will review the more common viral infections that can cause arthritic symptoms. An overview of pathogenesis and diagnosis of viral arthritis is presented separately. (See "Pathogenesis and diagnosis of viral arthritis".)
HEPATITIS A VIRUS
In hepatitis A virus (HAV) infections, arthralgias and rash occur in 10 to 14 percent of patients, but arthritis is extremely rare and there is some suspicion that patients with arthritis attributed to HAV infection truly had hepatitis C (HCV). Arthritis has been described primarily in patients with vasculitis who had a chronic relapsing form of hepatitis A, and also high titer of polyclonal IgG- and IgM-circulating cryoglobulins (type III cryoglobulinemia) .
HEPATITIS B VIRUS
Individuals infected with the hepatitis B virus (HBV) can be either asymptomatic or symptomatic. Asymptomatic infection is more common than the latter, especially in young children. Most primary infections in adults are self-limited, with clearance of the virus from the blood and liver and the development of lasting immunity to reinfection [2,3]. However, some primary infections in healthy adults, generally less than 5 percent, do not resolve, but develop into persistent infections. This is manifested by serological evidence of a primary infection by the appearance of hepatitis B surface antigen (HBsAg), followed shortly by IgM antibodies against HBV core antigen (anti-HBc antibodies); then circulating HBeAg becomes detectable.
Clinically, a prodromal phase of one to six months is followed by the onset of nonspecific symptoms including fever, nausea, vomiting, anorexia, and abdominal pain, which generally precedes the onset of icterus by 1 to 14 days [2,3]. In such cases, viral replication continues in the liver and there is continued viremia, although the titers of the virus in the liver and blood are variable.
People with subclinical persistent infection, normal serum aminotransferase levels, and nearly normal findings on liver biopsy are termed asymptomatic chronic HBV carriers; those with abnormal liver function and histologic features are classified as having chronic hepatitis B. During the prodromal phase and the early phase of clinical disease, HBsAg may be evident in the circulation. Only later does anti-HBsAg appear with a subsequent clearance of circulating viral products. Joint symptoms associated with HBV infections are believed to be due to the formation and deposition of immune complexes; cryoprecipitates containing HBsAg and complement components have been reported in affected patients [4,5]. Affected patients may have an earlier anti-HBsAg response, promoting immune complex formation .