The polymerase milieu of human papillomavirus

Abstract

High-risk human papillomaviruses (HPVs) cause cervical, anogenital, and head and neck cancers. A key oncogenic mechanism involves viral exploitation of host DNA damage tolerance pathways to support productive replication, a process that also drives genomic instability. Despite evidence that specific cellular polymerases participate in HPV genome replication, the full complement of polymerases deployed across the viral life cycle remains poorly defined. This minireview examines the potential roles of both replicative and translesion synthesis (TLS) polymerases at distinct stages of the HPV life cycle, and new tools that can be used to assess their potential importance in driving cancer, the life cycle, and altering mutagenic potential.