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Chikungunya virus (CHIKV) RNA is the infectious genetic material of the Chikungunya virus, a member of the Togaviridae family transmitted by Aedes mosquitoes (Silva & Dermody, 2017, Journal of Clinical Investigation). This positive-sense, single-stranded RNA genome is approximately 11.8 kilobases long and contains two main open reading frames that encode non-structural proteins (nsP1-4) and structural proteins (C, E3, E2, 6K, E1). Upon entering a host cell, the genomic RNA is immediately translated by host machinery to produce the viral replication complex, and it subsequently serves as the template for both negative-strand RNA intermediates and subgenomic RNA (Dash et al., 2008, Gene Therapy). As a therapeutic target, CHIKV RNA can be directly targeted by antisense oligonucleotides or small interfering RNAs (siRNAs) to trigger its degradation or by small molecule inhibitors like Favipiravir that induce lethal mutagenesis during replication (Delang et al., 2014, Antiviral Research). Additionally, compounds like Silvestrol can inhibit the translation of the viral RNA by targeting host factors like eIF4A (Henss et al., 2018, Antiviral Research). Effective targeting of CHIKV RNA is essential for controlling viral titers and preventing the progression of acute Chikungunya fever into chronic, debilitating polyarthralgia.
Inhibition of viral RNA synthesis via RNA-dependent RNA polymerase (RdRp) interference, induction of lethal mutagenesis within the RNA genome, RNA interference (RNAi) mediated degradation, and inhibition of RNA translation.
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