Chikungunya

• It is caused by a single-stranded RNA virus in the Alphavirus genus (Togaviridae).
• It is spread mainly by Aedes aegypti and Aedes albopictus mosquitoes. Humans are the main host during epidemics.
• Rare routes are bloodborne exposure and mother-to-baby transmission. The baby can be infected in utero, mostly in the second trimester, or at delivery if the mother is viremic. No cases have been reported through breastfeeding.
• One infection likely gives protection against future infection. (Red Book 2021, p. 449-450)

• The incubation period is 1 to 12 days, usually 2 to 3. (Tintinalli's Emergency Medicine)
• Most infected people develop symptoms. Onset is abrupt, with high fever (usually above 39°C) and polyarthralgia. The fever lasts several days to a week and can be biphasic.
• Joint pain is often severe and disabling. It is usually bilateral and symmetric, mostly in the hands and feet.
• Other features are headache, myalgia, conjunctivitis, nausea and vomiting, and a maculopapular rash. The rash can itch and usually involves the trunk and limbs, sometimes the palms, soles and face.
• Lab findings include lymphopenia, thrombocytopenia, raised creatinine and raised transaminases.
• The name comes from Kimakonde, meaning "to become contorted," which describes the stooped posture caused by joint pain. (Red Book 2021, p. 449)

• Rare but notable complications are meningoencephalitis, myelitis, Guillain-Barré syndrome and cranial nerve palsies. Others are uveitis, retinitis, myocarditis, hepatitis, nephritis, bullous skin lesions and hemorrhage.
• Neonates infected around birth, adults over 65, and people with hypertension, diabetes, or cardiovascular or kidney disease are at higher risk of severe disease.
• Chronic arthralgia, arthritis and tenosynovitis can last months to years. Risk factors are age over 50, arthritis in the acute phase, and a severe or prolonged initial illness. Mortality is rare.

• Diagnosis is by RT-PCR in the first week or so, then by IgM or neutralizing antibodies. (Tintinalli's and Red Book)
• Zika and dengue circulate in the same regions and look similar, so test for them too in travelers returning from the tropics.

• Treatment is supportive: rest, fluids and acetaminophen.
• Avoid NSAIDs and aspirin until dengue has been excluded.
• Persistent arthritis may need NSAIDs, or rheumatology input for DMARDs.
• Prevention relies on mosquito avoidance and vector control.

Vaccines (recent changes)

• Ixchiq (Valneva, live-attenuated):
  • The US FDA suspended its license in August 2025 because of serious adverse reactions.
  • In February 2026 the UK MHRA contraindicated it for adults over 60 and for people with hypertension, cardiovascular disease, diabetes or chronic kidney disease.
  • On 20 October 2026 the MHRA withdrew its UK license. It cited chikungunya-like illness and rare neurological events, including encephalitis, some leading to hospitalization or death. (Reported by The Pharmaceutical Journal.)
• Vimkunya (Bavarian Nordic, non-replicating virus-like particle):
  • It is now the only licensed UK option, approved for ages 12 and over.
  • In trials, 98% of people aged 12 to 64 developed neutralizing antibodies at day 22. This fell to 86% at 6 months.
• A 2026 systematic review (PMID 41564838) compares the immunogenicity and safety of the two vaccines. I haven't read its full text.

Chikungunya pathology

1. Virus

• CHIKV is an enveloped, positive-strand RNA alphavirus of about 12 kb, in the Togaviridae family. Aedes aegypti and Ae. albopictus transmit it. (Firestein & Kelley's Rheumatology, p. 2556)
• Other alphaviruses that cause arthritis are O'nyong-nyong, Ross River, Sindbis, Mayaro and Semliki Forest virus.

2. Entry, cell targets and viremia

• Receptor: The entry receptor is mxra8 (matrix remodeling associated 8, also called limitrin). It binds a surface-exposed domain of the viral envelope protein. (Firestein)
• Main target: Fibroblasts are the main cells that CHIKV infects and replicates in. This includes human synovial and skin fibroblasts. (Firestein)
• Other targets: The virus also infects endothelial and epithelial cells, hepatocytes, neurons, astrocytes, muscle satellite cells and osteoblasts. (Firestein)
• Partial resistance: Resting fibroblasts and a CD141+/CD90+ subset of synovial fibroblasts resist infection to some degree.
• Viremia: Viremia is brief, usually 5 to 7 days. Type I interferon and antibodies mainly control it. (Firestein)
• Early disease: Most early manifestations come from the high viremia. It drives an intense inflammatory response, with immune cells infiltrating the joints and surrounding tissues. (Fitzpatrick's Dermatology, p. 3170)
• Joint pain: Direct infection of osteoblasts may help explain the arthralgia and arthritis. (Fitzpatrick's)

3. Joint and musculoskeletal pathology

• Acute stage: Synovitis and tenosynovitis develop, with infiltration of monocytes and macrophages.
• Chronic stage:
  • Viral antigen and RNA persist in macrophages for up to 90 days. In one patient, viral RNA and protein were found in synovial macrophages 18 months after infection. (Fitzpatrick's, p. 3170)
  • One study found no detectable viral persistence in synovial fluid at 22 months. The persistence mechanism is therefore not settled.
• Imaging: MRI findings include joint effusion, bone erosion, marrow edema, synovial thickening, tendonitis and tenosynovitis. Ultrasound often shows tenosynovitis or enthesopathy rather than true synovitis. (Firestein)
• Chronic arthritis: Some patients progress to erosive arthritis 1 to 2 years after infection. RF and anti-CCP are usually negative, so the picture looks like RA but is not classic seropositive RA. About one third of patients with joint pain in one study met ACR criteria for RA. (Firestein)
• Chronic pain: The pain is probably partly neuropathic as well as nociceptive. Patients often respond poorly to ordinary analgesics. (Firestein)
• Predictors of non-recovery: These are age over 45, severe initial joint pain, and underlying osteoarthritis. (Firestein)

4. Skin pathology

• Morbilliform rash: It affects 40 to 50% of patients, or more in some series, and may leave islands of sparing. Later hyperpigmentation is common. (Andrews' Diseases of the Skin; Fitzpatrick's)
• Bullous disease in infants:
  • It occurs mostly in infants under 1 year. Blisters are flaccid, Nikolsky sign is positive, and the picture can resemble toxic epidermal necrolysis, with up to 80% of body surface area denuded.
  • Biopsy: It shows an intraepidermal blister with free-floating acantholytic cells.
  • Virus in the blister: Viral titers in blister fluid exceed those in blood. (Andrews')
• Other skin findings: Aphthous-like ulcers, acral lymphedema, and neuropathic acral changes (Raynaud-like, erythromelalgia) as late sequelae.

5. Other organs

• Nervous system: Meningoencephalitis, myelitis, Guillain-Barré syndrome and cranial nerve palsies.
• Other organs: Myocarditis, hepatitis, nephritis, uveitis and retinitis. (Red Book 2021)
• Lab changes: Lymphopenia, thrombocytopenia, and raised creatinine and transaminases.
• Perinatal infection: Vertical transmission can cause severe neonatal disease.

Images

Limits of this answer

• The library textbooks I found don't describe tissue histology of the synovium or other organs beyond the skin biopsy above.
• Recent PubMed searches on pathogenesis returned only bibliometric and drug reviews, with nothing that contradicts the textbook account.
• I can go deeper on the immunopathology of chronic arthritis (cytokines, T cells, and how it differs from RA) if you want.