Version July 2025
INTRODUCTION —
Chikungunya virus is an arthropod-borne alphavirus transmitted by mosquitoes that causes acute febrile polyarthralgia and inflammatory arthritis, as well as cutaneous eruptions and other systemic manifestations [1]. Further, many patients develop chronic joint involvement. In these patients, treatment with immunomodulatory or immunosuppressive drugs may achieve disease control. The name chikungunya is derived from an African language and means "that which bends up" or "stooped walk" because of the incapacitating joint involvement that may complicate the disease.
The treatment and prevention of chikungunya fever are discussed here. The epidemiology, clinical manifestations, and diagnosis of chikungunya infection are discussed separately. (See "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis".)
Issues related to other viral causes of arthritis are also presented separately. (See "Viral arthritis: Causes and approach to evaluation and management".)
TREATMENT —
Treatment is influenced by the phase and duration of the illness and the response to therapy. Acute disease, including both articular and nonarticular disease, is typically treated symptomatically and if needed, with supportive measures. (See 'Acute disease' below.)
Following the acute phase, most patients who remain symptomatic have joint disease; chronic joint disease may benefit from disease-modifying antirheumatic drugs (DMARDs) commonly used to manage other forms of chronic inflammatory arthritis, such as rheumatoid arthritis (RA). (See 'Post-acute and chronic arthritis' below.)
Inflammatory arthritis evident on physical examination and chronic arthralgia without physical findings are treated similarly; the latter is also presumed to be due to ongoing inflammatory synovitis, although this is based upon limited evidence.
Most descriptions of disease and their sequelae rely upon data from large outbreaks. Persistent and sometimes severe polyarthralgia is the most prominent feature, often without the swelling and erythema on examination that would suggest ongoing inflammation. Diffuse joint stiffness is also a prominent feature associated with disability in this population [2]. These patients typically have prolonged morning stiffness and may respond to conventional synthetic DMARDs (csDMARDs), suggesting an ongoing inflammatory arthritis as the underlying cause.
Moreover, a few ultrasound studies have demonstrated inflammatory synovitis in patients during the acute phase of infection [3] and in those with both post-acute and chronic joint pain [4]. However, few studies of these populations include synovial fluid analysis or histology [5,6] or explore whether acute arthritis should be treated differently than chronic arthralgia and chronic arthritis. (See "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)
Acute disease — Treatment during the acute phase of disease consists of supportive care with rest and fluids. It may include acetaminophen, followed as needed by nonsteroidal antiinflammatory drugs (NSAIDs). There is no specific antiviral therapy for acute chikungunya virus infection [7-9].
The acute illness typically lasts approximately 7 to 10 days, but acute disease requiring treatment may persist up to a month. In patients with clinical manifestations of acute chikungunya infection (eg, acute pain, fever, and arthralgia), we suggest acetaminophen (paracetamol; up to 500 to 1000 mg three times daily) or, once dengue is excluded and if acetaminophen is inadequate for symptom relief, NSAIDs (eg, naproxen 375 to 500 mg twice daily, ibuprofen 400 to 800 mg three times daily, or another NSAID); any NSAID may be used.
Typically, an NSAID trial should last two weeks, and if ineffective, patients should be switched to a different NSAID. Both acetaminophen and NSAIDs should be used in the lowest dose and for the shortest duration necessary and avoided in patients with contraindications including known liver disease or elevated aminotransferases. There is no evidence that any one NSAID is superior to another or that in chikungunya infection, any specific NSAIDs should be avoided. Contraindications to NSAIDs and adverse effects of these agents (including renal, gastrointestinal, and cardiovascular disease) are discussed in detail separately. (See "Nonselective NSAIDs: Overview of adverse effects" and "Overview of COX-2 selective NSAIDs", section on 'Toxicities and possible toxicities'.)
In a patient who could have dengue virus infection, aspirin and other NSAIDs should not be used until dengue has been excluded or until 14 days after symptom onset, with the patient afebrile ≥48 hours and no warning signs for severe dengue (severe abdominal pain, persistent vomiting, mucosal bleeding, pleural effusion or ascites, lethargy, enlarged liver, and increased hematocrit with decrease in platelet count). This is important given the risk of bleeding complications associated with dengue infection, which could be worsened by aspirin or other NSAIDs, and because of the potential risk of Reye syndrome in children treated with salicylates. Coinfection with dengue and chikungunya viruses can occur, so acute dengue infection must be excluded even if chikungunya infection is confirmed. The diagnosis of dengue fever, chikungunya fever, and related diagnoses are described separately. (See "Dengue virus infection: Prevention and treatment" and "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Diagnosis' and "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Differential diagnosis'.)
In patients with acute disease and severe pain who are unable to take acetaminophen and NSAIDs, or who do not respond adequately to these agents, we selectively use opioid analgesics (eg, tramadol or oxycodone) in the lowest dose for the shortest duration necessary.
In general, systemic glucocorticoids and other immunosuppressive medications should be avoided during acute infection. The safety of immunosuppression during acute infection is not well established, and there is concern that use of these agents may exacerbate the infection, especially during the viremic phase, which lasts approximately nine days [9]. (See "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Acute infection'.)
In patients with acute chikungunya fever, the rash resolves spontaneously and does not require treatment, although itching or burning can be treated symptomatically with topical calamine lotion and antihistamines [10].
Most patients experience improvement in symptoms within a month, regardless of therapy. Hospitalization is required infrequently, typically in infants, older adults, or immunocompromised patients with organ-threatening disease or severe complications related to an underlying medical condition.
Our treatment approach is based upon reports from case series [7,8], our clinical experience, and recommendations from expert groups [9,11]. There are only a few randomized trials; they have a number of limitations [12]. As examples:
●Treatment with daily NSAIDs and glucocorticoids (beginning in the second week of acute illness) has been associated with some symptomatic benefit during the first six weeks of illness. In one trial involving 120 patients with acute chikungunya fever and arthritis, patients randomly assigned to treatment for six weeks with either aceclofenac (an NSAID) monotherapy (200 mg daily), aceclofenac plus hydroxychloroquine (HCQ; 400 mg daily), aceclofenac plus prednisolone (10 mg daily), or aceclofenac plus HCQ plus prednisolone, all groups showed benefit from therapy and had increased difficulty performing activities of daily living upon discontinuation of medications at week 6 [13]. Greater pain relief was observed among the patients who received prednisolone compared with the patients who did not receive prednisolone (an approximate reduction in pain scores from baseline of 75 versus 30 to 40 percent).
●Limited evidence demonstrates no benefit of chloroquine or HCQ in patients with acute symptoms. In a randomized trial involving 54 patients, there was no improvement in acute or chronic pain or in the level of viremia in the first three days in patients receiving chloroquine compared with placebo [14]. In this report, it was unclear whether the patients were being treated during the acute and/or subacute phase of infection. Greater pain was reported at day 200 among patients who received chloroquine.
Post-acute and chronic arthritis — Management of persistent or relapsed manifestations, particularly joint disease, depends upon the duration of the symptoms. Symptomatic control of articular manifestations with antiinflammatory drugs and analgesics is appropriate in the several months immediately following the acute phase of disease. More chronic disease (beyond three months after onset of infection) may require the use of DMARD therapy, such as methotrexate (MTX).
For patients who present with severe post-acute or chronic symptoms, it is important to confirm chikungunya virus infection by establishing that patients are seropositive (positive anti-chikungunya virus immunoglobulin G [IgG]). Furthermore, other types of arthritis must be excluded (eg, RA, seronegative spondyloarthritis [SpA], or crystalline arthritis) before attributing symptoms to chikungunya virus. (See "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Diagnosis' and "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Differential diagnosis'.)
Post-acute arthritis — In patients with joint symptoms persisting into the post-acute phase (between one month and up to the end of the third month after onset of infection), we suggest continued analgesia (eg, acetaminophen) and, if needed, NSAIDs. (See 'Acute disease' above.)
As in patients with acute symptoms, the minimal necessary dose and duration of medications is used. Periodically, an effort should be made to reduce and discontinue medications. Joint symptoms may gradually resolve over several months, and ongoing treatment may no longer be required.
In patients whose symptoms are refractory to two to three two-week courses of different NSAIDs and who exhibit arthralgia or arthritis, tendinitis, or bursitis, especially those with evidence of severe synovitis and joint swelling and persistent elevation of inflammatory markers, we suggest systemic glucocorticoids (prednisone 10 to 20 mg daily for five days, depending upon severity, tapered over 10 days). We give the lowest effective glucocorticoid dose possible with a short trial, which is sometimes sufficient; however, the individual response to therapy varies substantially; more severely affected patients may require higher doses (0.5 mg/kg daily) [9], and some patients require up to one to two months of glucocorticoid therapy [15]. One expert guideline suggests limiting glucocorticoids when possible to no more than four weeks of therapy [9].
Intraarticular glucocorticoids are rarely, if ever, indicated because the usual pattern of joint involvement is polyarticular, with involvement of multiple small and large joints, and because there is no evidence to support the efficacy of this approach.
Neuropathic pain is common after chikungunya infection. Additional analgesic benefit may be provided by use of medications for neuropathic pain (eg, pregabalin or gabapentin) (see "Overview of pharmacologic management of chronic pain in adults", section on 'Antiseizure medications'). Physical therapy may also be helpful.
The approach to patients who develop Raynaud phenomenon is the same as in other patients with this disorder. (See "Treatment of Raynaud phenomenon: Initial management".)
Our treatment approach is based upon reports from case series, our clinical experience, and recommendations from expert groups [9,11]. Randomized trials are lacking or have limitations and limited applicability [12,16].
Indications for referral — Patients with clinical manifestations (particularly suspected inflammatory arthritis) that persist at least three months after the onset of infection should be referred to a rheumatologist for evaluation and initiation and management of DMARD therapy if appropriate.
Chronic arthritis — The approach to therapy in chronic arthritis (duration >3 months after infection) is similar to management of other chronic inflammatory arthritides. MTX has been the most commonly used DMARD, typically using the same approach as in RA (see "Initial treatment of rheumatoid arthritis in adults"). There is more limited experience using sulfasalazine (SSZ) (see "Treatment of peripheral spondyloarthritis"). DMARD combinations have been used in some patients [17], and tumor necrosis factor (TNF) inhibitors have been effective in patients resistant to or unable to take MTX [18,19]. (See 'Initial therapy of chronic arthritis' below and 'Resistant to initial therapy for chronic arthritis' below and 'Duration of therapy' below.)
Initial therapy of chronic arthritis — Chronic arthritis occurs as a continuation of the subacute disease, and patients will generally have been treated with acetaminophen and usually NSAIDs by this point in their illness (see 'Post-acute arthritis' above). Some patients may be receiving glucocorticoids or require initiation of glucocorticoids, as in post-acute disease (see 'Post-acute arthritis' above), to control symptoms until DMARDs are effective.
In patients with chronic arthritis not controlled by NSAIDs or prednisone 5 to 7.5 mg daily (or equivalent), we suggest a csDMARD, usually MTX; SSZ or an alternative DMARD are other options, as described below. For patients on NSAIDs or glucocorticoids, periodic attempts (eg, monthly) should be made to taper therapy, given the natural history of gradual improvement over months in chronic chikungunya arthritis. Similarly, we discontinue MTX (or other DMARDs) within several months after patients respond. (See "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis", section on 'Chronic arthritis and arthralgia' and "Major adverse effects of systemic glucocorticoids".)
Limited evidence suggests that MTX is the best available DMARD for patients with chronic chikungunya arthritis:
●Chronic peripheral arthritis – In most patients with chronic peripheral arthritis, especially that which resembles RA, who require ongoing therapy for symptomatic control, we suggest MTX, using the approach described in detail separately for patients with RA (see "Initial treatment of rheumatoid arthritis in adults" and "Use of methotrexate in the treatment of rheumatoid arthritis"). The adverse effects of MTX are described separately as well. (See "Major adverse effects of low-dose methotrexate".)
Low-dose MTX (ie, 15 mg to 25 mg once per week) is often sufficient to control symptoms. At doses of MTX higher than 15 mg weekly, absorption can by optimized through subcutaneous administration or split oral doses (two doses 8 to 12 hours apart once weekly), as is done for patients with RA. MTX requires careful laboratory monitoring (eg, for cytopenias, transaminitis) and must be used with caution in individuals with chronic kidney disease; it should never be used in individuals with end-stage kidney disease. (See "Use of methotrexate in the treatment of rheumatoid arthritis", section on 'Alternatives to once-weekly oral therapy'.)
Alternatives to MTX in patients unable to take the drug include SSZ, as well as other csDMARDs, but there is little evidence to support the use of csDMARDs other than MTX and SSZ. Several studies suggest that HCQ is ineffective [13,14,16]. (See "Initial treatment of rheumatoid arthritis in adults".)
●Chronic axial spondyloarthritis pattern – In patients with disease of the axial spine, in whom MTX may not be effective, we suggest a TNF inhibitor, using the approach described in detail separately for patients with axial SpA (see "Treatment of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Inadequate response to NSAIDs'). This approach is based upon clinical experience and indirect evidence from the use of TNF inhibitors for the treatment of axial SpA, and patients should be closely monitored given the very limited safety data for the use of biologic DMARDs (bDMARDs) in the setting of this viral infection. Available information regarding the adverse effects of TNF inhibitor therapy is described in detail separately. (See "Tumor necrosis factor-alpha inhibitors: An overview of adverse effects".)
Our treatment approach is based on the available, primarily observational data [8,15,18,20,21] and expert opinion [9,11,22] that suggest a benefit with MTX. As an example, in one of the largest retrospective observational studies, among 72 patients treated with MTX 15 mg weekly, a positive therapeutic response (no need for dose escalation or a switch in therapy) was observed in patients with chronic RA, SpA, and undifferentiated polyarthritis disease patterns (67, 80, and 100 percent of patients, respectively) [8].
However, limited data inform the efficacy of MTX compared with other interventions for chronic arthritis following chikungunya infection [12]. Several small randomized trials have methodologic issues that reduce confidence in the findings or have failed to detect a difference. One randomized trial of 72 patients with HCQ-refractory chronic arthritis found greater improvement in pain, disease activity, and disability after six months of triple therapy (MTX 15 mg once weekly plus SSZ 1 gram daily plus HCQ 400 mg daily) compared with continued HCQ monotherapy [17]. However, that trial was open-label, possibly confounding the findings; some patients also received prednisolone (7.5 mg daily, tapered off over six weeks) and acetaminophen or NSAIDs. Another randomized trial of 60 patients with chronic arthritis found similar rates of remission at six months in patients who received low-dose MTX (10 to 25 mg weekly) and patients who received NSAIDs (86 and 93 percent, respectively) [23]. A separate randomized trial of 31 patients found similar symptomatic improvements in patients treated with MTX (20 mg weekly) and dexamethasone compared with the patients who received dexamethasone and placebo [24].
Evidence is also lacking as to whether therapy protects against joint injury. Still, the available supporting evidence, combined with established risks of alternatives (eg, chronic glucocorticoids), suggest that MTX is warranted in patients with chronic polyarthritis [25,26]. Well-designed randomized trials are needed to compare MTX with other agents.
Small trials using chloroquine or HCQ for post-acute or chronic arthritis have not shown benefit and have limitations in study design.
Resistant to initial therapy for chronic arthritis — The approach to patients with an inadequate response to at least three months of initial DMARD therapy depends upon the drugs that have already been tried and perhaps the pattern of joint involvement; evidence to guide treatment in this population is lacking. Reasonable strategies include the following:
●Resistant to MTX – Arthritis resistant to MTX monotherapy could be treated with combination therapy with other csDMARDs [17] or with an alternative csDMARD, such as SSZ or leflunomide. We do not use HCQ monotherapy. For patients in whom csDMARDs are ineffective, one expert group recommends a TNF inhibitor among the bDMARDs, although the safety of bDMARDs has not been established in these patients [11]. Two cohort studies suggest TNF inhibitors are associated with symptom improvement and slower progression of structural damage [19,27]. (See "Initial treatment of rheumatoid arthritis in adults".)
●Resistant to SSZ – In patients with chronic polyarthritis (RA-like disease) that is resistant to SSZ, MTX would be a preferred option (see 'Initial therapy of chronic arthritis' above). In patients with SpA-like disease, MTX would be an option if no significant axial involvement is present, but a TNF inhibitor would be preferred in patients with symptomatic axial involvement.
bDMARDs such as TNF inhibitors have not been rigorously studied in chronic chikungunya arthritis, but they have been used in some refractory cases [8].
Duration of therapy — In patients with a complete response for at least six months, we attempt to discontinue DMARD therapy. This is consistent with the approach suggested by an expert panel, which recommended that DMARDs may be discontinued in most patients following symptom resolution [9]. However, this approach has not been systematically studied, and the optimal approach remains to be determined. We also prioritize discontinuation of glucocorticoids, but resume treatment if active disease recurs.
Patients with pre-existing rheumatic disease — The management of pre-existing rheumatic disease during acute chikungunya infection requires precaution regarding medications that increase risk of bleeding until dengue is excluded and immunosuppressive medications that could worsen viremia (see 'Acute disease' above). Otherwise, treatment of the patient's pre-existing rheumatic condition is unchanged.
In one small case series, patients with pre-existing inflammatory rheumatic diseases on csDMARDs and bDMARDs, including TNF inhibitors, were managed effectively with NSAIDs and rest; in spite of DMARD therapy, they experienced a normal course of chikungunya infection without exacerbation of their pre-existing rheumatic disease [28].
PROGNOSIS —
Nearly all patients with chikungunya arthritis eventually recover, although the duration of chronic symptoms varies widely. In one prospective study, the predictors of chronicity were age >40, severity of acute disease, and underlying osteoarthritis [8]. Some studies have reported progressive joint injury [29], and there are ongoing studies attempting to define the long-term implications of the disease. An observational study from La Réunion found that 17 out of 30 patients who had been diagnosed with chikungunya virus-induced arthritis continued to have persistent inflammatory joint symptoms 13 years later [27]. In these patients, there was no evidence of seroconversion to anti-cyclic citrullinated peptide (CCP) or rheumatoid factor (RF) positivity. Generally, joint damage due to chronic chikungunya arthritis typically has not been visible by radiography but has been appreciable by magnetic resonance imaging (MRI) in a subset of patients [30].
PREVENTION
Mosquito protection — Prevention of chikungunya virus infection consists of minimizing mosquito exposure [31]. Aedes mosquitoes bite primarily during the daytime; they breed in standing water (particularly containers) [32]. Measures to avoid mosquito bites include personal protection and environmental control measures. (See "Prevention of arthropod bites: Repellents and other measures" and "Zika virus infection: An overview", section on 'Mosquito protection'.)
Individuals with chikungunya infection may reduce spread of infection to others by following precautions to avoid mosquito bites during the first week of illness (the likely period of viremia).
Vaccination
Available chikungunya vaccine — The US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) have approved two chikungunya vaccines. IXCHIQ (also known as VLA1553) is a live-attenuated chikungunya vaccine approved for individuals 18 years and older [33,34]. VIMKUNYA (also known as CHIKV VLP) is a recombinant chikungunya virus vaccine using a virus-like particle (VLP) vaccine approved in 2025 for individuals 12 years and older [35,36].
In the United States, the Advisory Committee on Immunization Practices (ACIP) suggested chikungunya vaccine with IXCHIQ for selected high-risk travelers and selected high-risk laboratory workers. The ACIP has voted on the use of VIMKUNYA, although the recommendations are not formal policy [37].
Live-attenuated vaccine (IXCHIQ) — IXCHIQ (also known as VLA1553) is a live-attenuated chikungunya vaccine approved in 2024 by the FDA and the EMA for individuals 18 years and older [33,34]. It is administered as a single intramuscular dose.
In the United States, we agree with the ACIP, which suggests chikungunya vaccine with IXCHIQ in the following situations [38]:
●Selected high-risk travelers – Indications for vaccination of travelers are discussed in detail elsewhere. (See "Immunizations for travel", section on 'Chikungunya vaccine'.)
●Selected high-risk laboratory workers – These comprise workers with potential for specific exposure to chikungunya virus (eg, through research) but do not include exposure through routinely handling of clinical samples under standard precautions.
Contraindications (eg, immunocompromising conditions, anaphylaxis) and precautions (eg, with regards to pregnancy) are discussed in detail elsewhere. (See "Immunizations for travel", section on 'Chikungunya vaccine'.)
Support for IXCHIQ comes from trials demonstrating immunogenicity. Efficacy trials are lacking. In a double-blind trial based in the United States in which healthy adults (age ≥18 years) were randomly assigned to a single dose of vaccine or placebo, 362 patients were initially assessed for immunogenicity [39]. A seroprotective neutralizing antibody response occurred by 28 days in 99 percent of those who received vaccine and persisted in 96 percent at 180 days. None of the placebo recipients developed a neutralizing antibody response. Longitudinal follow-up of 363 participants who had received IXCHIQ in this trial confirmed persistence of protective levels of neutralizing antibodies in 97 percent at two years [40]. Antibody response rates were similar among participants aged 18 to 64 years and among those 65 years and older.
Similarly, in a double-blind, randomized trial among adolescents aged 12 to <18 years in Brazil, the chikungunya vaccine induced protective neutralizing antibodies in 99 percent of baseline seronegative individuals [41]. Among baseline seropositive individuals, protective antibody responses increased from 96 to 100 percent after vaccination.
The vaccine is generally well tolerated, although some recipients have transient symptoms similar to those seen with chikungunya infection. In the trial from the United States, the most common adverse effects in adults included headache (32 percent), fatigue (29 percent), myalgia (24 percent), arthralgia (18 percent), and fever (14 percent) [39]. Two serious adverse effects were attributed to the vaccine (myalgia and syndrome of inappropriate antidiuretic hormone secretion), both of which resolved.
A similar adverse effect profile was seen among adolescents; the arthralgias were short lived with a median duration of one day (range one to five days) [41].
Further studies are needed focusing on vaccine efficacy, cross-protection against multiple chikungunya virus strains, duration of immunity, and safety and efficacy in other populations, such as children and pregnant women.
Recombinant vaccine (VIMKUNYA) — VIMKUNYA (also known as CHIKV VLP) is a recombinant chikungunya vaccine based on a VLP that was approved by the FDA and EMA in 2025 for individuals 12 years and older. It is administered as a single intramuscular dose. The ACIP and the European Commission final recommendations for use are pending.
Support for CHIKV VLP comes from several clinical trials demonstrating a favorable safety profile and sustained immunogenicity at six months across diverse patient populations ranging from young adolescents to adults 65 years and older [42-45]. In an unpublished randomized, double-blind, placebo-controlled trial of 3454 participants aged 12 to 64 years, single-dose CHIKV VLP induced a seroprotective antibody response at day 22 and at six months in 98 and 86 percent of patients, respectively [42]. In another unpublished randomized, double-blind, placebo-controlled trial of 413 participants aged 65 years and older, a single dose induced a seroprotective response at day 22 and at six months in 87 and 76 percent of patients, respectively [43].
Pre-existing immunity has the potential to impact vaccine efficacy and safety, and impaired immune responses have been observed after sequential alphavirus vaccination (including the live chikungunya vaccine) [46,47]. However, in an open-label randomized trial in the United States, CHIKV VLP vaccine produced similarly potent immunogenicity in 30 alphavirus-vaccine naïve participants compared with 30 recipients who had previously been vaccinated with a heterologous alphavirus vaccine (an investigational Venezuelan equine encephalitis virus vaccine) [44]. Although both groups achieved 100 percent seroconversion by day 22, immune responses developed more quickly in prior alphavirus vaccinees (a fourfold increase in neutralizing antibodies occurred by day 8 in 93 percent compared with 67 percent of alphavirus-naïve controls).
In these trials, CHIKV VLP vaccine was well tolerated. Most adverse events were self-limited and grade 1 or 2 in severity, including injection site pain, fatigue, headache, and myalgia. No vaccine-related serious adverse events or deaths occurred.
Vaccine development — Development of other types of vaccines for prevention of chikungunya virus infection is also underway [48-53]:
●In a randomized trial including more than 260 healthy adults in non-chikungunya-endemic regions, a live-attenuated, measles-vectored vaccine expressing chikungunya virus structural proteins (MV-CHIK), or a measles vaccine prime and MV-CHIK, induced neutralizing antibodies against chikungunya virus after one or two immunizations [53]. Seroconversion rates in those who received MV-CHIK ranged from 50 to 93 percent after one dose and 86 to 100 percent after two doses. Immune responses were durable up to six months after one or two doses and the vaccine was safe and well-tolerated. Additional clinical trials are ongoing.
●A messenger RNA (mRNA)-based vaccine (VLA-181388) is in phase 1 clinical trials [54,55].
SUMMARY AND RECOMMENDATIONS
●Supportive care – There is no specific antiviral therapy for treatment of chikungunya virus infection, and management during the acute phase is supportive, including rest, fluids, and antiinflammatory and analgesic agents (see 'Acute disease' above):
•In patients in whom dengue has been excluded, we suggest NSAIDs (eg, naproxen 375 to 500 mg twice daily, ibuprofen 400 to 800 mg three times daily, or another NSAID) rather than glucocorticoids for symptomatic relief (Grade 2C). Any NSAID may be used.
•Aspirin and other NSAIDs are avoided initially if dengue has not been excluded because of the risk of bleeding complications. Acetaminophen (paracetamol; up to 500 to 1000 mg three times daily) can be used in this setting. Aspirin should also be avoided in children because of the potential risk of Reye syndrome.
●Refractory arthritis – For patients not responsive to two to three two-week courses of NSAIDs who exhibit musculoskeletal symptoms, particularly patients with severe synovitis, joint swelling, or persistent elevation of inflammatory markers, we suggest systemic glucocorticoids (Grade 2C). A typical initial dose is prednisone 10 to 20 mg daily for five days, depending upon severity, then tapered off over the next 10 days. More severely affected patients may require higher doses (eg, prednisone 0.5 mg/kg daily), and some patients require up to one to two months of glucocorticoid therapy. We use the lowest effective dose possible. (See 'Post-acute arthritis' above.)
●Chronic arthritis – For patients with chronic arthritis (>3 months after initial infection) who are unable to taper prednisone without recurrence of symptoms, we suggest treatment with a disease-modifying antirheumatic drug (DMARD; eg, methotrexate [MTX], or if MTX is contraindicated, sulfasalazine [SSZ]), rather than continuing glucocorticoids alone (Grade 2C). The choice of DMARD may be guided by the pattern of joint involvement. We generally use the same approach to dosing and monitoring these medications as in RA but make an effort to taper medications once patients have been asymptomatic for at least six months. (See 'Chronic arthritis' above.)
•Polyarthritis resembling rheumatoid arthritis – For most patients with persistent RA-like chronic polyarthritis, we suggest MTX (Grade 2C). We use the approach described in detail separately for patients with RA, with initial titration of MTX to 15 to 25 mg once weekly. (See "Initial treatment of rheumatoid arthritis in adults" and "Use of methotrexate in the treatment of rheumatoid arthritis".)
For patients unable to take MTX, alternatives include SSZ and other conventional synthetic DMARDs (csDMARDs) as discussed separately. (See "Initial treatment of rheumatoid arthritis in adults".)
•Axial arthritis – For patients with disease of the axial spine, we suggest a tumor necrosis factor (TNF) inhibitor (Grade 2C). The approach is the same as for patients with axial SpA, which is described in detail separately (see "Treatment of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Inadequate response to NSAIDs'). Patients should be closely monitored given the lack of safety data for the use of these biologic DMARDs in the setting of this viral infection.
●Prevention
•Mosquito protection – Minimizing mosquito exposure is the cornerstone of prevention. Individuals with chikungunya infection may reduce spread of infection to others by following precautions to avoid mosquito bites during the first week of illness (the likely window of viremia). (See 'Prevention' above.)
•Vaccination – One type of live-attenuated vaccine to prevent infection with chikungunya virus (VLA1553, or IXCHIQ) is available in the United States and Europe for persons 18 years and older. Use in travelers is discussed elsewhere. A virus-like particle (VLP) vaccine (VIMKUNYA) is also available in the United States and Europe. Development and regulatory review of other vaccine candidates is ongoing. (See 'Vaccination' above and "Immunizations for travel", section on 'Chikungunya vaccine'.)
ACKNOWLEDGMENTS —
The UpToDate editorial staff acknowledges Jonathan J Miner, MD, PhD, and Deborah Lenschow, MD, PhD, who contributed to earlier versions of this topic review.
