Viral arthritis

The role of viruses in the development of acute and chronic arthritis is complex, because viruses are ubiquitous, and all human beings are occasionally afflicted by viral infections. In general, most viral infections (ie, most respiratory pathogens) are acute and self-limiting and survive by infecting one susceptible host, then moving on to another. Some viruses establish prolonged latency in the host after acute infection, resulting in clinical symptoms after many years of dormancy, such as dermatomal zoster following chicken pox. Still other viral agents produce chronic infections following the primary stage in all (HIV), most (hepatitis C virus), or a minority (hepatitis B virus) of the infected. The mechanisms whereby these infections produce arthritis are diverse and still poorly understood, but are clearly influenced by both host and viral factors. In rubella, viral infection within the joint is probably responsible. For hepatitis B and C, arthritis may result directly from host cellular or humoral immune responses, while other viruses may act indirectly by altering the integrated host defense network, or by inducing frank autoimmunity, as with HIV and HTLV-1. Although viral arthritis is usually self-limited and nondestructive, chronic forms arise in two settings. First, chronic viral arthritis may occur when immunodeficient patients are infected with agents that are short-lived pathogens in normal hosts, leading to chronic or recurrent infection, with arthritis as one sequela. Second, chronic arthritis may also occur with infections that are by their very nature chronic persistent viral illnesses. This review addresses these and other common forms of viral arthritis, such as that caused by parvovirus B19.