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Chikungunya can cause joint pain. Is it true that there is no treatment for Chikungunya joint pain? How do patients normally cope with it?

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It is true that there is no treatment for the Chikungunya virus and infection. That is not the same as there being no treatment for the pain. The CDC recommends acetaminophen but not aspirin or NSAIDs for the fever and pain.

Wikipedia says:

Symptoms usually improve within a week; however, occasionally the joint pain may last for months. The risk of death is around 1 in 1,000.

People either cope with the pain for a week or more, or take Tylenol for it until it goes away.

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Kate Gregory's answer is perfect, but I wanted to expound a little bit on the "is it true that there is no treatment for Chikungunya joint pain" part of your question. James Crowe is a very interesting physician-scientist who focuses on what he calls "generalized medicine," a sort-of opposite to personalized medicine – instead of sequencing millions of individual genomes to find some shared target, his lab finds rare antibodies in single individuals who have survived or shown uncommon resistance to diseases with no known cures. In 2015, his group isolated several candidate antibodies from an individual who recovered from their Chikungunya infection. (Emphasis mine.)

Isolation and Characterization of Broad and Ultrapotent Human Monoclonal Antibodies with Therapeutic Activity against Chikungunya Virus. Smith et al. Cell Host & Microbe. 2015.

Chikungunya virus (CHIKV) is a mosquito-transmitted RNA virus that causes acute febrile infection associated with polyarthralgia in humans. Mechanisms of protective immunity against CHIKV are poorly understood, and no effective therapeutics or vaccines are available. We isolated and characterized human monoclonal antibodies (mAbs) that neutralize CHIKV infectivity. Among the 30 mAbs isolated, 13 had broad and ultrapotent neutralizing activity (IC50 < 10 ng/ml), and all of these mapped to domain A of the E2 envelope protein. Potent inhibitory mAbs blocked post-attachment steps required for CHIKV membrane fusion, and several were protective in a lethal challenge model in immunocompromised mice, even when administered at late time points after infection. These highly protective mAbs could be considered for prevention or treatment of CHIKV infection, and their epitope location in domain A of E2 could be targeted for rational structure-based vaccine development.

In 2017, an animal trial showed that their "engineered SVIR001, a recombinant fully human monoclonal antibody (mAb)...eliminated viremia, reduced viral load at the site of infection, and diminished spread to distant target tissues in rhesus macaques when administered after infection," so there might be an imminent antibody therapy for Chikungunya, although these are often very expensive.

Therapeutic administration of a recombinant human monoclonal antibody reduces the severity of chikungunya virus disease in rhesus macaques. Broeckel et al. PLOS Neglected Tropical Diseases. 2017.

Chikungunya virus (CHIKV) is a mosquito-borne virus that causes a febrile syndrome in humans associated with acute and chronic debilitating joint and muscle pain. Currently no licensed vaccines or therapeutics are available to prevent or treat CHIKV infections. We recently isolated a panel of potently neutralizing human monoclonal antibodies (mAbs), one (4N12) of which exhibited prophylactic and post-exposure therapeutic activity against CHIKV in immunocompromised mice. Here, we describe the development of an engineered CHIKV mAb, designated SVIR001, that has similar antigen binding and neutralization profiles to its parent, 4N12. Because therapeutic administration of SVIR001 in immunocompetent mice significantly reduced viral load in joint tissues, we evaluated its efficacy in a rhesus macaque model of CHIKV infection. Rhesus macaques that were treated after infection with SVIR001 showed rapid elimination of viremia and less severe joint infiltration and disease compared to animals treated with SVIR002, an isotype control mAb. SVIR001 reduced viral burden at the site of infection and at distant sites and also diminished the numbers of activated innate immune cells and levels of pro-inflammatory cytokines and chemokines. SVIR001 therapy; however, did not substantively reduce the induction of CHIKV-specific B or T cell responses. Collectively, these results show promising therapeutic activity of a human anti-CHIKV mAb in rhesus macaques and provide proof-of-principle for its possible use in humans to treat active CHIKV infections.

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