Viral infections are estimated to cause up to 10% of all cancers worldwide, of which nearly 50% are attributable to infection with a high-risk human papillomavirus (HPV). HPV drives cervical cancer and subsets of other anogenital cancers and head and neck cancers. HPV integration is associated with structural variation (SV) and dysregulation of both the HPV and human genomes, both of which have been difficult to resolve using short-read sequencing. We recently reported distinct patterns of genomic regulation around HPV integration events in cervical cancer using Oxford Nanopore Technologies (ONT) long-read sequencing in a paper published in Genome Research (Porter et al. 2024, doi:10.1101/gr.279041.124). We profiled 72 tumors from the HIV+ Tumor Molecular Characterization Project (HTMCP) and categorized HPV integration events based on patterns of HPV / human genome rearrangements. We observed complex HPV integration structures, in some cases involving heterologous amplifications of HPV-human concatemers, and methylation and gene expression changes in cis with the HPV-integrated allele. We are continuing this work in cervical cancer as well as in vulvar cancer and in head and neck cancer. The head and neck cancer samples come from the personalized approaches in the treatment of head and neck cancers (PATH) study, of which a subset of cases are driven by Epstein-barr virus (EBV) in addition to HPV+ and virus-negative cases (see PATH study page). Given the endemic nature of HPV and its association with cancers in populations around the world, it is important for us to understand how HPV disrupts genome structure and function and contributes to malignant progression.