NGS Analysis Human Papillomavirus Type 18 E2 DNA-Binding Domain Bound to its DNA Target with Biopython

Abstract

Cervical cancer, a significant global health concern, is primarily caused by persistent infection with high-risk human papillomavirus (HPV) types, particularly HPV18. The E2 DNA-binding domain (DBD) of HPV-18 plays a crucial role in regulating viral replication and transcription. Disrupting the function of this domain can significantly impact the viral lifecycle, thereby preventing the progression of cervical cancer. By studying the molecular interactions between the E2 DNA-binding domain and its DNA target, the research aims to identify potential therapeutic targets and provide a framework for developing targeted treatments. This study leverages high-throughput sequencing technologies to decode proteomics data, illuminating critical genetic information and gene expression patterns. Through the multifaceted application of advanced bioinformatics tools, including sequence analysis using BLAST; multiple sequence alignment with CLUSTAL Omega and COBALT; protein domain and motif identification via InterProScan; structural analysis using CATH and PDBSum; and visualization with Jalview, we dissected the molecular mechanisms underpinning cancer pathogenesis. Furthermore, the study determined proteolytic cleavage site prediction by Expasy Peptide Cutter; and identified potential immunogenic regions within the E2 DBD using an in-silico tool, IEDB B and T-cell epitope. This integrated approach provides insights into the structural and functional properties of the HPV18 E2 DBD and its interaction with DNA, as well as potential implications for immunotherapeutic strategies targeting this critical viral protein. Additionally, Biopython was employed for bioinformatics analyses, enabling seamless data integration and processing to enhance the prediction accuracy of immunogenic regions and further characterize the E2 DBD. Through the application of NGS and bioinformatics tools, the study provides a thorough investigation of the molecular interactions and mechanisms by which the HPV-18 E2 DBD influences the pathogenesis of cervical cancer. By identifying key interactions and potential therapeutic targets, this research lays the groundwork for developing targeted treatments that can effectively disrupt the viral lifecycle and reduce the risk of cervical cancer.