Editorial: Lessons Learned From Chikungunya in the Americas

In 2013, chikungunya virus arrived in the Western Hemisphere, spreading like wildfire across the islands of the Caribbean, Mexico, Central America, and South America, resulting in ~3 million infections (1). Similar to historical outbreaks in the Eastern Hemisphere, chikungunya virus spread quickly in a population without preexisting immunity. The chikungunya virus outbreak also created new challenges for rheumatologists, who were suddenly encountering a disease entity with which there was little familiarity. Included among these challenges was identifying the factors that predispose patients to the development of chronic arthritis, understanding the pathogenesis driving persistent arthritis, and determining treatments that would be efficacious and safe in patients with chikungunya arthritis. In this issue of Arthritis & Rheumatology, two new studies and a review address some new discoveries from the chikungunya virus epidemic in the Americas and discuss lessons learned from prior outbreaks of chikungunya arthritis in the Eastern Hemisphere (2–4). Upon infection with chikungunya virus, ~90% of patients develop acute symptoms, which can include fever, inflammatory arthritis with morning stiffness, and severe pain throughout the first week after infection (5). Some patients also develop a rash and conjunctivitis during the acute phase of the illness. Severe cases can even cause viral encephalitis and occasionally death in neonates (6). Also of concern, especially to the rheumatologist, is the fact that many patients infected with chikungunya virus develop arthralgias and arthritis, which can persist for up to 3 years (7). The mechanisms underlying persistent chikungunya arthritis remain a mystery and are an area of active scientific investigation. Alphaviruses are enveloped, single-stranded positive sense RNA viruses belonging to the Togaviridae family (5). Alphaviruses can be divided into New World alphaviruses that typically cause encephalitis (e.g., Western equine encephalitis virus) and Old World alphaviruses that cause viral arthritis (e.g., chikungunya virus and Ross River virus). Like some other arthritogenic alphaviruses, chikungunya virus is spread by Aedes mosquitos, and in particular A aegypti, which is found primarily in tropical and subtropical climates. Numerous epidemiologic studies were published in the wake of the 2006 chikungunya virus epidemic on R eunion Island, where approximately one-third of the island’s population was infected (6,8–11). Those studies defined the frequency of acute and chronic manifestations of disease in the Eastern Hemisphere. However, less was known about epidemiologic outcomes of the chikungunya virus outbreak in the Americas. In one of their studies published in this issue of Arthritis & Rheumatology, Chang et al (2) set out to determine the frequency of chronic joint pain after chikungunya virus infection in a Colombian cohort. The authors enrolled 485 serologically confirmed cases and clinically reevaluated the patients 20 months after infection. As noted in our study of a small cohort of chikungunya virus–infected American travelers to Haiti (12), the most commonly affected joints in the patients included the small joints of the distal extremities. At the 20-month follow-up the authors found that arthralgias were persistent in ~25% of the patients. They also identified some interesting correlates of persistent joint pain, including college graduate status, headache at onset of infection, and ≥4 weeks of initial pain, among others. There are several major implications of this study by Chang et al (2). First, the presence of persistent joint inflammation strongly suggests that the chikungunya virus strain that spread to the Americas caused a chronic arthritis disease phenotype similar to what was described in prior outbreaks in the Eastern Hemisphere. The authors also raised important limitations of the study. For example, Mayaro virus is an arthritogenic Old World Jonathan J. Miner, MD, PhD, Deborah J. Lenschow, MD, PhD: Washington University School of Medicine, St. Louis, Missouri. Address correspondence to Jonathan J. Miner, MD, PhD, or Deborah J. Lenschow, MD, PhD, Departments of Medicine, Molecular Microbiology, and Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, Box 8045, St. Louis, MO 63110. E-mail: jonathan.miner@wustl.edu or dlenschow@wustl.edu. Submitted for publication January 12, 2018; accepted January 16, 2018.