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Chikungunya virus (CHIKV), a reemerging arbovirus, causes a crippling musculoskeletal inflammatory disease in humans characterized by fever, polyarthralgia, myalgia, rash, and headache. CHIKV is transmitted by Aedes species of mosquitoes and is capable of an epidemic, urban transmission cycle with high rates of infection. Since 2004, CHIKV has spread to new areas, causing disease on a global scale, and the potential for CHIKV epidemics remains high. Although CHIKV has caused millions of cases of disease and significant economic burden in affected areas, no licensed vaccines or antiviral therapies are available. In this Review, we describe CHIKV epidemiology, replication cycle, pathogenesis and host immune responses, and prospects for effective vaccines and highlight important questions for future research.

Chikungunya virus (CHIKV) emerged in the Americas in late 2013 to cause substantial acute and chronic morbidity. About 1.1 million cases of chikungunya were reported within a year, including severe cases and deaths. The burden of chikungunya is unclear owing to inadequate disease surveillance and underdiagnosis. Virus evolution, globalization, and climate change may further CHIKV spread. No approved vaccine or antiviral therapeutics exist. Early detection and appropriate management could reduce the burden of severe atypical and chronic arthritic disease. Improved surveillance and risk assessment are needed to mitigate the impact of chikungunya.

In this review, we highlight biological characteristics of Aedes aegypti and Aedes albopictus, 2 invasive mosquito species and primary vectors of chikungunya virus (CHIKV), that set the tone of these species' invasiveness, vector competence, and vectorial capacity (VC). The invasiveness of both species, as well as their public health threats as vectors, is enhanced by preference for human blood. Vector competence, characterized by the efficiency of an ingested arbovirus to replicate and become infectious in the mosquito, depends largely on vector and virus genetics, and most A. aegypti and A. albopictus populations thus far tested confer vector competence for CHIKV. VC, an entomological analog of the pathogen's basic reproductive rate (R₀), is epidemiologically more important than vector competence but less frequently measured, owing to challenges in obtaining valid estimates of parameters such as vector survivorship and host feeding rates. Understanding the complexities of these factors will be pivotal in curbing CHIKV transmission.

Re-emergence of chikungunya virus, a mosquito-transmitted pathogen, is of serious public health concern. In the past 15 years, after decades of infrequent, sporadic outbreaks, the virus has caused major epidemic outbreaks in Africa, Asia, the Indian Ocean, and more recently the Caribbean and the Americas. Chikungunya virus is mainly transmitted by Aedes aegypti mosquitoes in tropical and subtropical regions, but the potential exists for further spread because of genetic adaptation of the virus to Aedes albopictus, a species that thrives in temperate regions. Chikungunya virus represents a substantial health burden to affected populations, with symptoms that include severe joint and muscle pain, rashes, and fever, as well as prolonged periods of disability in some patients. The inflammatory response coincides with raised levels of immune mediators and infiltration of immune cells into infected joints and surrounding tissues. Animal models have provided insights into disease pathology and immune responses. Although host innate and adaptive responses have a role in viral clearance and protection, they can also contribute to virus-induced immune pathology. Understanding the mechanisms of host immune responses is essential for the development of treatments and vaccines. Inhibitory compounds targeting key inflammatory pathways, as well as attenuated virus vaccines, have shown some success in animal models, including an attenuated vaccine strain based on an isolate from La Reunion incorporating an internal ribosome entry sequence that prevents the virus from infecting mosquitoes and a vaccine based on virus-like particles expressing envelope proteins. However, immune correlates of protection, as well as the safety of prophylactic and therapeutic candidates, are important to consider for their application in chikungunya infections. In this Review, we provide an update on chikungunya virus with regard to its epidemiology, molecular virology, virus-host interactions, immunological responses, animal models, and potential antiviral therapies and vaccines.

The largest epidemic ever recorded for chikungunya, a disease caused by infection with the chikungunya virus (CHIKV), began in Africa in 2004 and spread to >100 countries on four continents. The epidemic caused >10 million cases of often debilitating rheumatic disease, classically involving rapid onset of fever and polyarthralgia, often with polyarthritis. The clinical diagnosis of chikungunya is often complicated by infections with dengue or Zika virus. For many individuals with chikungunya, the disease is benign and self-limiting; however, some patients have a complex spectrum of atypical and severe manifestations. Many patients also experience a chronic phase of the disease, primarily involving arthralgia (which can be protracted (>1 year)), and a number of sequelae are also recognized. CHIKV-induced arthropathy arises from infection of multiple cell types in the joint and the infiltration of mainly mononuclear cells. Innate responses (primarily involving type I interferon responses and natural killer cells) and cognate responses (primarily involving CD4 T helper 1 cells), alongside activation of macrophages and monocytes, mediate CHIKV-induced arthritic immunopathology. Ideally, improved anti-inflammatory treatments should not compromise antiviral immunity. New concepts in mosquito control are being field tested and a number of CHIKV vaccines are being developed.

Chikungunya virus (CHIKV) is a globally re-emerging arbovirus for which previous studies have indicated the majority of infections result in symptomatic febrile illness. We sought to characterize the proportion of subclinical and symptomatic CHIKV infections in a prospective cohort study in a country with known CHIKV circulation. A prospective longitudinal cohort of subjects ≥6 months old underwent community-based active surveillance for acute febrile illness in Cebu City, Philippines from 2012-13. Subjects with fever history were clinically evaluated at acute, 2, 5, and 8 day visits, and at a 3-week convalescent visit. Blood was collected at the acute and 3-week convalescent visits. Symptomatic CHIKV infections were identified by positive CHIKV PCR in acute blood samples and/or CHIKV IgM/IgG ELISA seroconversion in paired acute/convalescent samples. Enrollment and 12-month blood samples underwent plaque reduction neutralization test (PRNT) using CHIKV attenuated strain 181/clone25. Subclinical CHIKV infections were identified by ≥8-fold rise from a baseline enrollment PRNT titer <10 without symptomatic infection detected during the intervening surveillance period. Selected CHIKV PCR-positive samples underwent viral isolation and envelope protein-1 gene sequencing. Of 853 subjects who completed all study procedures at 12 months, 19 symptomatic infections (2.19 per 100 person-years) and 87 subclinical infections (10.03 per 100 person-years) occurred. The ratio of subclinical-to-symptomatic infections was 4.6:1 varying with age from 2:1 in 6 month-5 year olds to 12:1 in those >50 years old. Baseline CHIKV PRNT titer ≥10 was associated with 100% (95%CI: 46.1, 100.0) protection from symptomatic CHIKV infection. Phylogenetic analysis demonstrated Asian genotype closely related to strains from Asia and the Caribbean. Subclinical infections accounted for a majority of total CHIKV infections. A positive baseline CHIKV PRNT titer was associated with protection from symptomatic CHIKV infection. These findings have implications for assessing disease burden, understanding virus transmission, and supporting vaccine development.

Chikungunya virus (CHIKV) is transmitted by Aedes aegypti and Aedes albopictus mosquitoes and causes febrile illness with severe arthralgia in humans. There are 3 circulating CHIKV genotypes, Asia, East/Central/South Africa, and West Africa. CHIKV was first reported in 1953 in Tanzania, and up until the early 2000s, a few outbreaks and sporadic cases of CHIKV were mainly reported in Africa and Asia. However, from 2004 to 2005, a large epidemic spanned from Kenya over to the southwestern Indian Ocean region, India, and Southeast Asia. Identified in 2005, the E1 glycoprotein A226V mutation of the East/Central/South Africa genotype conferred enhanced transmission by the A. albopictus mosquito and has been implicated in CHIKV's further spread in the last decade. In 2013, the Asian CHIKV genotype emerged in the Caribbean and quickly took the Americas by storm. This review will discuss the history of CHIKV as well as its expanding geographic distribution.

We conducted a cross-sectional serosurvey for chikungunya virus (CHIKV) exposure in fruit bats in Senegal during 2020-2023. We found that 13.3% (89/671) of bats had CHIKV IgG; highest prevalence was in Eidolon helvum (18.3%, 15/82) and Epomophorus gambianus (13.7%, 63/461) bats. Our results suggest these bats are naturally exposed to CHIKV.

Chikungunya virus infection often manifests as an acute, self-limiting febrile illness, with arthralgia and musculoskeletal symptoms being the most commonly reported. Arthralgia can persist for months or even years, and approximately 50% of cases progress to chronic conditions. However, recent outbreaks have revealed a rising number of severe cases and fatalities. This review examines evidence from the past decade that suggests a higher incidence of severe chikungunya virus (CHIKV) infections and increased mortality rates, challenging official reports and guidelines from many countries. The literature review includes case reports, series, and studies with comparison groups to assess whether CHIKV-related mortality is underreported. Evaluating excess mortality involves analyzing consistent findings across different regions, biological plausibility, and systemic manifestations that contribute to severe outcomes. These findings aim to expand disease classifications in international guidelines and raise awareness among healthcare professionals to better identify severe CHIKV cases and related deaths. Studies were identified through PubMed using the search terms “chikungunya”, “death”, “severe”, “pathogenesis”, and “pathophysiology”.

Numerous recent studies have illuminated global distributions of human cases of dengue and other mosquito-transmitted diseases, yet the potential distributions of key vector species have not been incorporated integrally into those mapping efforts. Projections onto future conditions to illuminate potential distributional shifts in coming decades are similarly lacking, at least outside Europe. This study examined the global potential distributions of Aedes aegypti and Aedes albopictus in relation to climatic variation worldwide to develop ecological niche models that, in turn, allowed anticipation of possible changes in distributional patterns into the future. Results indicated complex global rearrangements of potential distributional areas, which— given the impressive dispersal abilities of these two species—are likely to translate into actual distributional shifts. This exercise also signalled a crucial priority: digitization and sharing of existing distributional data so that models of this sort can be developed more rigorously, as present availability of such data is fragmentary and woefully incomplete.