In silico optimization of DNA codons in genes encoded by various strains of Ebola Virus

Abstract

Ebola hemorrhagic fever (HF) is a severe and often lethal disease that occurs in primates, including humans. It was first identified in 1976 during two outbreaks of fatal haemorrhagic fever in Central Africa. Due to its high fatality rate and lack of a widespread cure, Ebola HF poses a considerable challenge in treatment, making Ebola virus disease (EVD) one of the deadliest zoonotic diseases. The viral genome is [~]19kb long, linear, non-segmented, and negative single-stranded (-SS) RNA. The genome of the Ebola virus (EBOV) comprises seven genes, namely NP, GP, L, and VP (VP30, VP24, VP40, VP35), which encode nucleoprotein, glycoprotein, RNA polymerase, and viral proteins. By optimizing the DNA sequence through codon adaptation, we observed significant enhancements in the codon adaptation index (CAI) and the GC content compared to the wild-type strain. These findings demonstrate that optimized genes hold the potential for improved expression in the host organism without the production of truncated proteins. Further, these optimized genes can facilitate proper protein folding and function. In conclusion, these results have implications for vaccine production, as higher codon optimization enhances the expression of the genes, making them appropriate amounts for vaccine development.