Abstract
BackgroundPapillomaviruses (PVs) establish a persistent infection in the proliferating basal cells of the epithelium. The viral genome is replicated and maintained as a low-copy nuclear plasmid in basal keratinocytes. Bovine and human papillomaviruses (BPV and HPV) are known to utilize two viral proteins; E1, a DNA helicase, and E2, a transcription factor, which have been considered essential for viral DNA replication. However, growing evidence suggests that E1 and E2 are not entirely essential for stable replication of HPV.ResultsHere we report that multiple HPV16 mutants, lacking either or both E1 and E2 open reading frame (ORFs) and the long control region (LCR), still support extrachromosomal replication. Our data clearly indicate that HPV16 has a mode of replication, independent of viral trans-factors, E1 and E2, which is achieved by origin activity located outside of the LCR.
Highlights
Papillomaviruses (PVs) establish a persistent infection in the proliferating basal cells of the epithelium
Transient replication of HPV16 genomic DNA in different cell lines In order to determine the requirement for viral trans-factors in HPV16 DNA replication, different mammalian cell lines of epithelial or fibroblast lineage were examined for the ability to support transient viral DNA replication
These deletion mutants were examined for short-term replication using human epithelial cells, 293 and Human papillomavirus (HPV)-negative human cervical cells, C33A that were previously shown to support the replication of wild type (WT) HPV16
Summary
Papillomaviruses (PVs) establish a persistent infection in the proliferating basal cells of the epithelium. Papillomaviruses (PVs) infect the basal layers of epithelial cells and maintain their genomes at constant, but relatively low-copy number in basal epithelial cells. These viruses replicate their genomes as nuclear plasmids in their natural mammalian host cells. Short-term replication assays were performed in transformed cells, in order to identify the cis- and trans-elements that were required for replication of PVs [4]. Using this approach, with BPV1, the early proteins E1 and E2 were found to be required for viral DNA replication [5,6,7]. More detailed analyses have shown that the minimal BPV origin includes multiple E2BSs, an E1BS, and an AT-rich region [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
