Chikungunya infection: de-linking replication from symptomatology reveals the central role of muscle
Anne Moscona
Department of Pediatrics, Microbiology & Immunology, and Department of Physiology & Cellular Biophysics, Columbia University College of Physicians & Surgeons, New York, New York, USA.
Address correspondence to: Anne Moscona, 701 West 168th Street, New York, New York, 10032, USA. Phone: 347.366.2459; Email: am939@cumc.columbia.edu.
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First published February 10, 2020 - More info
J Clin Invest. 2020;130(3):1099–1101. https://doi.org/10.1172/JCI134746.
© 2020 American Society for Clinical Investigation
Chikungunya virus (CHIKV) is an emerging arbovirus, endemic in many parts of the world, that is spread by travelers and adapts to new mosquito vectors that live in temperate climates. CHIKV replicates in many host tissues and initially causes a self-limiting febrile illness similar to dengue. However, in 30%–40% of cases, CHIKV also causes long-term painful and debilitating muscle and joint pain, the pathogenesis of which remains unknown. In this issue of the JCI, Lentscher et al. engineered a skeletal muscle–restricted CHIKV to show that while musculoskeletal disease requires viral replication in affected muscle, muscular pathology is mediated by host immunological factors. These findings de-link viral replication and disease symptoms, illuminate the virus-host interplay in CHIKV symptomatology, and raise the possibility that immune modulation is a therapeutic option. The results also highlight possible solutions to existing vaccine barriers and provide insights that may apply to other viral diseases.
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