The virus is transmitted through mosquito bites
of ConsumerAffairsMay 22, 2025
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CHIKV can trigger long-term joint pain that mimics autoimmune diseases like rheumatoid arthritis, potentially due to sustained activity of CD4+ T cells.
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Researchers identified TNF-alphaan inflammatory molecule produced by CD4+ T cellsas a likely culprit in chronic inflammation.
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Findings may guide therapies that block TNF-alpha to relieve symptoms and prevent post-viral complications.
If youve developed joint pain you may suspect you are developing arthritis. On the other hand, it could be a mosquito bite.
A new study from researchers at the La Jolla Institute for Immunology has revealed a possible explanation for why some people infected with the Chikungunya virus (CHIKV) suffer long-term joint pain that mimics rheumatoid arthritis. Their findings may not only unlock a deeper understanding of the virus’s long-term health impacts but also point toward new therapeutic targets to prevent lasting pain.
The mosquito-borne CHIKV is known to cause short-term flu-like symptoms, but for some, the aftermath includes chronic joint pain that can persist for years. Scientists have long suspected an autoimmune component, but the biological mechanism behind it has remained elusiveuntil now.
In a study published in Cell Reports Medicine, LJI researchers investigated immune responses in CHIKV-infected individuals and discovered that a type of immune cell, the CD4+ T cell, appears to be the driving force behind the viruss long-term effects. Unlike typical anti-viral responses that feature a balance of both CD4+ helper and CD8+ killer T cells, this study found that CD4+ cells were significantly more active and more persistent.
“Autoimmune diseases like rheumatoid arthritis have exactly these parameters,” said Dr. Daniela Weiskopf, senior author and LJI assistant professor. This T-cell response looked awfully like what we see in autoimmune disease.
Inflammatory memory
The study focused on blood samples from CHIKV patients in Colombia and found that even six years after initial infection, 87% of patients still had CD4+ T cells that specifically recognized the virus. In contrast, only 13% retained CD8+ T cells. These CD4+ cells linger as memory cellsnormally a positive sign for immunitybut in this case, they may be causing harm.
The issue isnt just their persistence. The researchers found that many of these CD4+ cells were monofunctional, producing a single inflammatory moleculeTNF-alpha. While TNF-alpha is useful in fighting infections, its sustained presence long after viral clearance is a hallmark of autoimmune-like inflammation.
This kind of immune profile, dominated by CD4+ T cells producing TNF-alpha, is not typical for viral infectionsits something we see in diseases like rheumatoid arthritis, said Rimjhim Agarwal, study co-first author.
The findings open the door to potential treatments that block TNF-alpha, similar to those already used for autoimmune conditions.
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