At the University of Colorado Anschutz School of Medicine, immunologist Thomas Morrison has made a discovery that could finally explain why half of all people infected with chikungunya virus go on to suffer years of debilitating joint pain—and what might stop it. Working with his team including Kristen Zarrella, Ryan Sheridan, and Brian Ware, Morrison has found that the virus doesn't fully leave the body after the initial infection; instead, it hides inside joint-associated macrophages, specialized white blood cells that should be protecting us. The findings, published in Nature Microbiology, offer the first concrete explanation for chronic chikungunya arthritis, a condition that has puzzled researchers and devastated people across the globe.
Chikungunya virus has resurged dramatically in recent years, spread by infected Aedes mosquitoes. In just the first nine months of 2025, the World Health Organization reported more than 445,000 cases and 155 deaths across 40 countries. Most people infected experience the acute phase—high fever, intense joint swelling and pain, headache, and nausea—that typically arrives four to eight days after exposure. For about half of those people, symptoms fade within weeks, and life returns to normal. But for the other half, the joint pain and swelling persist for years, with no available treatment.
For years, scientists debated what caused the chronic progression. Some hypothesized the virus triggered an autoimmune response similar to rheumatoid arthritis, though supporting evidence remained inconclusive. Morrison and his lab pursued a different hypothesis: the virus itself never fully leaves the body. The immune system can control and clear the infection from many tissues, but in others—particularly the joints—the virus persists and continues to cause damage.
To understand exactly how this happens, Morrison's team employed cutting-edge techniques: single-cell RNA sequencing and spatial transcriptomics allowed them to map gene activity at the cellular level and identify precisely which cells in joint tissue were harboring the virus. The macrophages, it turned out, acted as a sanctuary. "The immune response is unable to clear it from certain tissues, and in this case, those are the joint-associated tissues," Morrison explains. Once the virus establishes itself in these specialized cells, the body's defenses cannot dislodge it, leading to chronic inflammation and relapsing arthralgia and arthritis that can span years.
Morrison emphasizes why this matters beyond laboratory walls. Chikungunya hits hardest in resource-limited regions of the world, where many people depend on physical work for their livelihood. Having chronic musculoskeletal pain isn't simply a matter of discomfort—it's a barrier to work, income, and dignity. Understanding the mechanism of persistence opens the door to new therapeutic approaches. The research was supported in part by the development of small molecule antivirals that can inhibit viral replication, suggesting that future treatments might prevent the virus from taking root in joint macrophages in the first place, or eliminate it once it does.
This work represents the first real breakthrough in understanding why chikungunya becomes chronic for so many. With more than 445,000 cases already reported in 2025, the implications for public health in affected regions could be profound.