{"title":"Codon Usage Bias Analysis of Human Papillomavirus 18s L1 Protein and its Host Adaptability","authors":"Vinaya Vinod Shinde, Swati Bankariya, Parminder Kaur","doi":"10.1101/2024.08.10.607454","DOIUrl":null,"url":null,"abstract":"Human Papillomavirus 18 (HPV 18) is known as a high-risk variant associated with cervical and anogenital malignancies. High-risk types HPV 18 and HPV 16 (human papillomavirus 16) play a major part in about 70 percent of cervical cancer worldwide (Ramakrishnan et al., 2015). The L1 protein of HPV 18 (HPV 18s L1 protein), also known as major capsid L1 protein is targeted in the vaccine development against HPV 18 due to its non-oncogenic and non-infectious properties with self-assembly ability into virus-like particles. In the present analysis, an extensive codon usage bias analysis of HPV 18s L1 protein and adaptation to its host human was conducted. The Effective number (Nc) Grand Average of Hydropathy (GRAVY), Index of Aromaticity (AROMO), and Codon Bias Index (CBI) values revealed no biases in codon usage of HPV 18s L1 protein. The data of the Codon Adaptation Index (CAI), and Relative Codon Deoptimization Index (RCDI) indicate adaptation of HPV 18s L1 protein according to its host human. The domination of selection pressure on codon usage of HPV 18s L1 protein was demonstrated based on GC12 vs GC3, Nc vs GC3, and frequency of optimal codons (FOP). The Parity plot revealed that the genome of HPV 18s L1 protein has a preference for purine over pyrimidine, that is G nucleotides over C, and no preference for A over T but A/T richness was observed in the genome of HPV 18s L1 protein. In the Nucleotide composition, GC1 richness ultimately represents evolutionary aspects of codon usage. Furthermore, these findings can be used in currently ongoing vaccine development and gene therapy to design viral vectors.","PeriodicalId":501307,"journal":{"name":"bioRxiv - Bioinformatics","volume":"37 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"bioRxiv - Bioinformatics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.08.10.607454","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Human Papillomavirus 18 (HPV 18) is known as a high-risk variant associated with cervical and anogenital malignancies. High-risk types HPV 18 and HPV 16 (human papillomavirus 16) play a major part in about 70 percent of cervical cancer worldwide (Ramakrishnan et al., 2015). The L1 protein of HPV 18 (HPV 18s L1 protein), also known as major capsid L1 protein is targeted in the vaccine development against HPV 18 due to its non-oncogenic and non-infectious properties with self-assembly ability into virus-like particles. In the present analysis, an extensive codon usage bias analysis of HPV 18s L1 protein and adaptation to its host human was conducted. The Effective number (Nc) Grand Average of Hydropathy (GRAVY), Index of Aromaticity (AROMO), and Codon Bias Index (CBI) values revealed no biases in codon usage of HPV 18s L1 protein. The data of the Codon Adaptation Index (CAI), and Relative Codon Deoptimization Index (RCDI) indicate adaptation of HPV 18s L1 protein according to its host human. The domination of selection pressure on codon usage of HPV 18s L1 protein was demonstrated based on GC12 vs GC3, Nc vs GC3, and frequency of optimal codons (FOP). The Parity plot revealed that the genome of HPV 18s L1 protein has a preference for purine over pyrimidine, that is G nucleotides over C, and no preference for A over T but A/T richness was observed in the genome of HPV 18s L1 protein. In the Nucleotide composition, GC1 richness ultimately represents evolutionary aspects of codon usage. Furthermore, these findings can be used in currently ongoing vaccine development and gene therapy to design viral vectors.