Chikungunya virus (CHIKV) is an enveloped, positive‑sense single‑stranded RNA virus that causes chikungunya fever, characterised by acute fever and debilitating joint pain. It belongs to the genus Alphavirus within the family Togaviridae. The spherical virion is about 70 nanometres in diameter and consists of an icosahedral nucleocapsid surrounded by a lipid envelope containing trimeric E1/E2 glycoprotein spikes.
Genome and Virology
The CHIKV genome is approximately 11.8 kilobases long and contains two open reading frames. The 5′ two-thirds of the genome encodes the nonstructural proteins nsP1–nsP4, which together form the viral replicase complex. The 3′ one-third encodes the structural polyprotein comprising the capsid, E3, E2, 6K/TF and E1 proteins, which is translated from a subgenomic RNA. After binding to host receptors such as the cell adhesion molecule MXRA8, the virus enters cells via clathrin-mediated endocytosis. Acidification of endosomes triggers E1-mediated membrane fusion, releasing the nucleocapsid into the cytoplasm. The genomic RNA acts as mRNA for translation of nonstructural proteins; replication occurs on cytoplasmic spherules formed at the plasma membrane, producing a negative‑sense RNA intermediate and new genomes. The subgenomic RNA drives synthesis of structural proteins. Capsid proteins encapsidate genomes and associate with E1/E2 glycoproteins at the plasma membrane, and new virions bud from the cell surface. CHIKV replicates in fibroblasts, muscle satellite cells and macrophages in humans and in the midguts and salivary glands of Aedes mosquitoes.
Outbreaks and Global Spread
CHIKV was first identified in Tanzania in 1952 and has since caused periodic outbreaks across Africa and Asia. There are three major genotypes: West African, East/Central/South African (ECSA) and Asian. A mutation (E1-A226V) in the ECSA lineage enhanced replication in Aedes albopictus, leading to explosive outbreaks in the Indian Ocean region between 2004 and 2006 and subsequent epidemics in India and Southeast Asia. The virus reached Europe in 2007, causing autochthonous transmission in Italy, and spread to the Caribbean in late 2013, igniting a large epidemic that extended to the Americas. Chikungunya fever is marked by abrupt onset of high fever, rash and severe polyarthralgia; chronic joint pain may persist for months or years in a subset of patients. Mortality is low but morbidity is high. There is no licensed antiviral therapy or vaccine; several vaccine candidates are in clinical development. Control efforts focus on reducing populations of Aedes aegypti and Aedes albopictus mosquitoes and preventing bites through personal protection and community-based vector management.
Chikungunya virus demonstrates how a mosquito-borne alphavirus can rapidly expand its geographic range and cause significant human disease through adaptation to new vectors.
Related Terms: Mayaro virus, Ross River virus, Dengue virus, Alphavirus, Aedes aegypti