The Immunobiology of viral arthritides

Abstract

A large range of human viruses are associated with the development of arthritis or arthralgia. Although there are many parallels with autoimmune arthritides, there is little evidence that viral arthritides lead to autoimmune disease. In humans viral arthritides usually last from weeks to months, can be debilitating, and are usually treated with non-steroidal anti-inflammatory drugs, but with variable success. Viral arthritides likely arise from immunopathological inflammatory responses directed at viruses and/or their products residing and/or replicating within joint tissues. Macrophages recruited by monocyte chemoattractant protein-1 (MCP-1/CCL2) and activated by interferon, and proinflammatory mediators like tumour necrosis factor α, interferon γ, interleukin-6 and interleukin-1β appear to be common elements in this group of diseases. The challenge for new treatments is to target excessive inflammation without compromising anti-viral immunity. Recent evidence from mouse models suggests targeting MCP-1 or complement may emerge as viable new treatment options for viral arthritides.