Arthritis and arthralgias are well-recognized and relatively common accompaniments to viral infections. The most common viruses causing arthritis and arthralgias are parvovirus, hepatitis B, hepatitis C, rubella, and the alphaviruses . Joint complaints are also observed less commonly in association with a wide variety of other viral infections (eg, mumps, enteroviruses, herpesviruses) (table 1) .
This topic will provide a general overview of the pathophysiology, presentation, diagnosis, and treatment of viral arthritis. Specific viruses that cause arthritis are discussed separately. (See "Specific viruses that cause arthritis".)
No virus has been implicated as a cause of the common forms of chronic inflammatory arthritis such as rheumatoid arthritis or systemic lupus erythematosus. However, viruses are able to initiate rheumatic symptoms via a variety of different mechanisms. Viruses may cause effects through numerous mechanisms that depend on host factors, including age, gender, genetics, infectious history, and immune response [1-5].
Direct invasion — Viruses may directly invade the joint, resulting in infection of the synovium or other joint tissues. This may be the mechanism utilized by rubella and rubella vaccine virus despite the fact that viral isolation from a joint is a rare occurrence [6-11]. In vivo data support the tropism of these viruses for synovial tissue and their potential for both lytic and persistent infection. Other viruses that may be arthrotropic include parvoviruses  and enteroviruses ; both of these have been successfully isolated from joint fluid.
Immune complex formation — Viral particles (either whole virions or viral antigens) may act as the antigenic component of immune complexes formed by the humoral response to viral infection [1,2,12,14]. These immune complexes may be preferentially deposited in the joints and skin, leading to arthralgias, arthritis, and rash. This type of presentation is common and has been well-documented in the cases of hepatitis B infection, alphaviruses, hepatitis C (often via the formation of cryoglobulins), and parvovirus. Antibodies directed against viral antigens also may crossreact with tissue antigens, a process called molecular mimicry [3,4].