The roles of DNA damage repair and innate immune surveillance pathways in HPV pathogenesis.

Human papillomaviruses (HPV) infect epithelial tissues and induce a variety of proliferative lesions. A subset of HPV types are also the causative agents of many anogenital as well as oropharyngeal cancers. Following infection of basal epithelial cells, HPVs establish their genomes as episomes in undifferentiated cells and require differentiation for their productive life cycles. During HPV infections, viral oncoproteins alter cellular pathways such as those for DNA damage repair and innate immune surveillances to regulate their productive life cycles. These pathways provide potential targets for therapeutic intervention.