Tracking Replicating HPV Genomes in Proliferating Keratinocytes

Jonathan R. Shin, Ivan Avilov, Mario Schelhaas, Franck Gallardo, Alison A. McBride
2025 · doi:10.1101/2025.03.18.644043
preprint OA: closed Public-Domain
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This paper developed a live-cell molecular tool to monitor replication and segregation of HPV18 genomes in keratinocytes by inserting the ANCHOR cis element into the HPV18 late region and expressing ParB-GFP from an HPV18-dependent replicon. The authors report that the resulting small replicon, containing the HPV18 replication origin and viral transcriptional enhancer, can replicate stably in keratinocytes when complemented by the HPV18 genome and minimally triggers innate immune activation, with neomycin resistance used for selection. Using fluorescent detection, they visualized partitioning in dividing cells and found HPV18-ANCH3 genomes were distributed somewhat equally to daughter cells, consistent with random attachment to host chromosomes. The study’s key limitation is that it tracks indirect fluorescent signals from an engineered replicon/ANCH3 system rather than native full viral genome dynamics. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract Human papillomavirus (HPV) genomes replicate and partition as minichromosomes alongside host chromatin during persistent infection. However, it is difficult to monitor genome dynamics in living cells because the small and compact genome will not easily tolerate expression cassettes. Here, we use ANCHOR™ technology to detect HPV18 genomes in living cells. We incorporated the cis element from ANCHORTM technology into the late region of the HPV18 genome and expressed the ParB-GFP protein from an HPV18-dependent replicon. The replicon contains the HPV18 replication origin and viral transcriptional enhancer element and can replicate stably in keratinocytes when complemented by the HPV18 genome. This small replicon expresses the neomycin resistance gene in both bacteria and eukaryotic cells and has minimal prokaryotic elements that could induce innate immunity. This molecular tool enables us to indirectly monitor the presence of the virus by detecting these fluorescent proteins in live cells and allows for real-time tracking of replicating HPV18-ANCH3 genomes in proliferating keratinocytes to inform on models of HPV genome maintenance, tethering, and amplification. Here, we visualize partitioning of the viral DNA in dividing cells and show that HPV18-ANCH genomes are distributed somewhat equally to daughter cells by random attachment to host chromosomes. Importance In persistent HPV infection, the viral genome is maintained at a constant copy number, replicates in synchrony with host DNA during S-phase, and is partitioned into daughter cells. The exact method by which HPVs partition to daughter cells is not well understood and the elucidation of such mechanisms may reveal relevant pharmacological targets to combat persistent HPV infection. Competing Interest Statement The authors have declared no competing interest.

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License: Public-Domain