Geovana Martelossi-Cebinelli, Jessica Aparecida Carneiro, Kelly Megumi Yaekashi, Mariana M. Bertozzi, Beatriz H. S. Bianchini, Fernanda S. Rasquel‐Oliveira, Camila Zanluca, Claudia Nunes Duarte dos Santos, Rachel Arredondo, T.R. Blackburn, Rúbia Casagrande, Waldiceu A. Verri
mosquitoes. Since its identification, CHIKV remained confined to parts of Africa and Asia until the early 2000s, when it expanded to other continents, causing epidemics. Structurally, it is an enveloped virus with a positive-single-stranded RNA genome, which encodes four non-structural proteins (nsP1-nsP4), responsible for viral replication, and five structural proteins (C, E3, E2, 6K, and E1), which form the capsid and envelope. Of these proteins, glycoproteins E1 and E2 are essential for cell recognition and membrane fusion, determining infectivity and viral tropism. CHIKV replication occurs in the cytosol of different cell types, triggering an intense inflammatory and immune response, which manifests clinically as Chikungunya fever (CHIKF). Despite its epidemiological impact, current treatment is limited to symptomatic approaches, including the use of analgesics and anti-inflammatories, as no specific antiviral therapies are available. In response, promising advances are being made, including the development of vaccines, targeted antivirals, and immunotherapies. This article aims to review the main aspects of viral biology, epidemiology, and immunopathogenesis of CHIKV infection, in addition to discussing the main advances in the development of new therapeutic approaches for its control.