Abstract
The Chikungunya virus (CHIKV) has emerged as a public health concern around the world as they have large epidemics. These epidemics are associated not just with mild but also with severe clinical manifestations. CHIKV was first discovered in Tanzania in 1952. Because of climate change, urbanization, and international travel, it has expanded. The rising incidence of diseases primarily transmitted by Aedes aegypti and Aedes albopictus mosquitoes highlights the urgent need for better surveillance, vector control, and therapeutics. CHIKV is an RNA virus that mutates frequently leading to genetic diversity and complicating disease management. In this review, we present how genomic variations of CHIKV can affect clinical presentation and transmission dynamics. We discuss the mutations in CHIKV that were analyzed in various outbreaks. We examine the structural and lifecycle characteristics of CHIKV, followed by a detailed exploration of important genomic modifications in structural (E1, E2) and nonstructural (nsP3) proteins, and their consequences for viral propagation, immune evasion, and pathogenicity. Mutations in the E1 protein, for instance, enhance entry into host cells, while mutations in the E2 protein reduce antibody neutralization. Changes in nsP3 are connected to more replication and disease problems. It is difficult to diagnose, treat, and make vaccines for them. The continuous genetic monitoring of viruses is important to check the new variants that are emerging. A comprehensive approach including better diagnostics, selective vector control, vaccine development, and community-based management would help mitigate CHIKV impact. Through illuminating the link between viral evolution and clinical outcomes, the current review aims to stimulate future research and reinforce preparedness against this ever-evolving virus.