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Human papillomaviruses (HPVs) establish long-term infections in patients. The mechanism for extrachromosomal HPV DNA persistence in cycling cells is unknown. We show that HPV origin-containing plasmids partition as minichromosomes, attributable to an association of the viral origin recognition protein E2 with mitotic spindles. alpha-, beta-, and gamma-tubulins were pulled down with a tagged E2. The N-terminal transacting and C-terminal protein dimerization/DNA binding domains independently associated with the spindles. We suggest that this E2 property enables these viruses to establish persistence. Its implication for HPV oncogenesis is presented.

Human papillomavirus (HPV) origin-binding protein associates with mitotic spindles to enable viral DNA partitioning