Comprehensive codon usage analysis of the African Swine Fever Virus

The non-uniform usage of synonymous codons occurs in genomes of all organisms, including DNA and RNA viruses. The preferential selection of a codon at the expense of other synonymous codons within the same group is known as Codon Usage Bias. The understanding of this bias assists in unveiling the factors driving molecular evolution, as defined by the selection-mutation-drift theory. According to this model, molecular evolution is predominantly driven by mutation, natural selection, and genetic drift. Nevertheless, elements like nucleotide composition, gene length, and protein secondary structure also contribute to this process. Comprehensive genomic analyses that highlight the codon usage preference of the African Swine Fever Virus (ASFV) are infrequent. ASFV, a hemorrhagic and highly contagious viral disease, almost invariably results in 100% fatality among infected pigs and wild boars. This study, therefore, embarked on a thorough examination of codon usage patterns in ASFV’s complete genomic sequences, an endeavor of great relevance to molecular evolution studies, complex transmission models, and vaccine research. For an exhaustive evaluation of ASFV’s whole-genome codon usage, we used parameters like ENC, RSCU, and CAI. A Principal Component Analysis was carried out to reaffirm the interconnected RSCU lineages based on the continent, and their evolutionary relationships were later elucidated through phylogenetic tree construction. ASFV emerged as a low-biased codon user (ENC = 52.8) that is moderately adapted to its host. Its genome has a high AT composition (64.05%), suggesting the impact of mutational pressure on genomic evolution. However, neutrality plot analysis revealed natural selection’s slight supremacy over mutational pressure. The low codon bias (>45) implies ASFV’s diverse usage of synonymous codons within a given codon family, allowing for effective translation and subsequent successful viral replication cycles. Its moderate adaptation (CAI = 0.56) permits the virus to infect a range of hosts, including reservoirs such as warthogs and bush pigs. To the best of our knowledge, this is the pioneering report providing a comprehensive examination of ASFV’s complete genomic sequences. Consequently, research focusing on viral gene expression and regulation, gene function prediction, parasite-host interaction, immune dysfunction, and drug and vaccine design may find this report to be a valuable resource.