Human papillomaviruses (HPVs) drive cervical cancer development, and integration of viral DNA into the host genome occurs in over 80% of patients. HPV integration is considered a key step in disease progression, and is associated with genomic, transcriptomic, and epigenetic dysregulation; however, its effect on 3D genome structure and function is unknown. We hypothesize that (1) HPV integration disrupts the 3D organization of the host genome, leading to pathogenic rewiring of genetic regulatory networks, and also that (2) 3D genome organization may inform or constrain HPV-mediated dysregulation. To address this, we are leveraging a well-characterized dataset of cervical cancer samples and integrating matched data from a variety of sequencing modalities. This work is expected to deepen our understanding of the multi-omic dysregulation mediated by HPV integration and the interplay between them, and potentially identify novel vulnerabilities for targeted therapies.