Abstract
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. α, β-, and γ-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.
Original language | English |
---|---|
Pages (from-to) | 4030-4035 |
Number of pages | 6 |
Journal | Proceedings of the National Academy of Sciences of the United States of America |
Volume | 101 |
Issue number | 12 |
DOIs | |
State | Published - Mar 23 2004 |