Acute-onset polyarticular arthritis is the most common presentation of viral arthritis. The most common viruses causing arthritis and/or arthralgias are parvovirus, the alphaviruses, hepatitis B, hepatitis C, Epstein-Barr virus (EBV), and tropical viruses, such as Zika and chikungunya (CHIKV). The diagnosis can be difficult to confirm but should be considered in all patients presenting with acute-onset polyarticular symptoms. Although viruses cause only a small proportion of all cases of acute arthritis, differentiation of virally mediated arthritis from primary rheumatological disease is important. Low-titer autoantibodies, such as rheumatoid factor and antinuclear antibody, can occur in the context of acute viral arthritis.
Many viruses could be responsible for causing viral arthritis, the most common being Parvovirus, alphavirus, rubella, Hepatitis B, C, and flavivirus. Some other viruses can also cause arthritis/arthralgia rarely. These are EBV, HIV, mumps, herpes, and cytomegalovirus (CMV). Recently, there has been an increase in the occurrence of mosquito-borne virus related arthropathies, such as the ones associated with Zika and CHIKV. Occasionally, the virus causing arthritis could be related to the patient co-morbidities. For example, EBV causing viral arthritis in patients on immunosuppressive agents.
Viral arthritis is reported worldwide, but the exact incidence and prevalence are unknown. This could be related to the multitude of viruses causing the arthritis syndrome, geographic variability, and more often than not, the self-limited nature of the illness.
In the majority of patients with viral arthritis, the mechanisms are poorly understood. Viruses can initiate articular symptoms via different mechanisms. These include the direct invasion of the joint, immune complex formation, and immune modulation causing chronic inflammation. The joint synovium is considered home for many arthritis-causing viruses which can recruit inflammatory cells to the joints and result in the inflammation cascade to continue. For example, in cases related to the alphaviruses, infected macrophages in the synovium are thought to be responsible for much of the pathology and inflammation through the release of pro-inflammatory cytokines and matrix metalloproteinases. They can further transfer these viruses to the resident cells such as synovial fibroblasts which, in turn, continue the inflammation cycle.
The constellation of signs and symptoms related to viral arthritis seems to be related to the specific virus causing the infection. As a rule, patients with viral arthritis present with a self-limited episode of symmetric polyarticular arthritis or arthralgia. Monoarthritis is unusual. The presentation might involve fever, rash, and lymphadenopathy. In rare cases, viral arthritis can mimic the presentation of rheumatic diseases like rheumatoid arthritis, especially because these viral arthritis syndromes could be associated with the presence of autoantibodies, namely rheumatoid factor (RF) and antinuclear antibody (ANA). The titers are usually low and disappear quickly. Some viruses, like CHIKV, are known to produce recurrent and many times chronic arthritis, but the majority of these infections are self-limiting, lasting less than 6 to 12 weeks.
Clinical Presentation and Pathophysiology Related to Individual Viral Entity
There is no single test or clinical presentation which is suggestive of viral arthritis. The diagnosis is mainly clinical, supported by other tests including inflammatory markers, autoantibodies, and serology. A viral etiology should be suspected in a patient presenting with acute onset of arthralgias or polyarticular symptoms especially if the duration of symptomatology has been less than six weeks. The presence of extra-articular symptoms viz rash or lymphadenopathy should be noted. Testing for antinuclear antibodies (ANA) rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA) could be helpful if the features of inflammatory arthritis persist. In suspected cases of viral arthritis, serum should be collected for serology. Serologic testing, however, must be directed against the specific viruses suspected based upon both epidemiologic and clinical data. As a general rule with serology, an IgM antibody response would be indicative of an acute infection and would be converted to IgG isotype after a few weeks. Due to the high rate of infections in the general population for example with EBV and hepatitis, positive IgG antibodies especially if stable in titers, are non-diagnostic. Other laboratory features are related to the specific viral syndromes. For example, the detection of positive HBsAg, elevated aminotransferases, and IgM anti-HBc antibodies in a patient with recent onset polyarthritis could provide the clue to the diagnosis of HBV-associated polyarthritis. Isolation of virus from the joint itself or viral cultures are not useful except in rare circumstances.
Treatment in viral arthritis is generally symptomatic. NSAIDs and acetaminophen should be used for pain and inflammation. The use of corticosteroids is usually discouraged and not recommended. In some cases, as in arthritis related to Hepatitis B/C or HIV, anti-viral treatment alone can lead to the resolution of the joint symptoms.
Viral arthritis is uncommon but should be strongly considered in the differential diagnosis of polyarticular joint pain for less than six weeks. High-risk groups include travelers from the endemic areas, healthcare workers, and IV drug abusers and should be especially considered. The early diagnosis and management are crucial for arboviruses; for example, Chikungunya from a public health and epidemiological perspective. [Level V] It should be recognized that many of these viral arthritis syndromes are associated with elevated markers of inflammation, namely rheumatoid factors and antinuclear antibodies. As mentioned, the titers for these markers are usually low and transient. Many of these cases can be managed in a primary care setting; however, if the arthralgia and joint swelling persist or worsen, referral to a rheumatologist would be prudent. [Level V]