Evidence map›Paper›PMID 19247434›Full record

ArticlePLoS pathogens2009

Establishment of human papillomavirus infection requires cell cycle progression.

Dohun Pyeon, Shane M Pearce, Simon M Lank, Paul Ahlquist, Paul F Lambert

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers.

0numbers the graph read from it
0cells of the map it votes in
230citing papers in PubMed
8.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

230 citing papers in PubMed, 345 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Viral interference of nucleocytoplasmic transport.The Journal of biological chemistry · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. E2 Tyrosine 102 Regulates MmuPV1 Pathogenesis In Vivo.Pathogens (Basel, Switzerland) · 2025
    Article
  19. bioRxiv : the preprint server for biology · 2025
    Article
  20. Article

170 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Dohun PyeonMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI, USA.
Shane M Pearce
Simon M Lank
Paul Ahlquist
Paul F Lambert
University of Wisconsin–Madison · USHoward Hughes Medical Institute · US

Funding

Visualizing EBV and HCMV DNA Dynamics During InfectionP01CA022443 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI WILLIAM M. SUGDEN · 1985 to 2026
$53.1M
Identification and Preclinical Testing of MicrobicidesR33AI071947 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI LAMBERT, PAUL F. · 2008 to 2010
$1.4M
Identification and Preclinical Testing of MicrobicidesR21AI071947 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI LAMBERT, PAUL F. · 2006 to 2007
$392k
Howard Hughes Medical InstituteNCI NIH HHS CA022443NCI NIH HHS P01 CA022443NIAID NIH HHS AI071947NIAID NIH HHS R21 AI071947NIAID NIH HHS R33 AI071947
6 · The paper itself

Abstract

Human papillomaviruses (HPVs) are DNA viruses associated with major human cancers. As such there is a strong interest in developing new means, such as vaccines and microbicides, to prevent HPV infections. Developing the latter requires a better understanding of the infectious life cycle of HPVs. The HPV infectious life cycle is closely linked to the differentiation state of the stratified epithelium it infects, with progeny virus only made in the terminally differentiating suprabasal compartment. It has long been recognized that HPV must first establish its infection within the basal layer of stratified epithelium, but why this is the case has not been understood. In part this restriction might reflect specificity of expression of entry receptors. However, this hypothesis could not fully explain the differentiation restriction of HPV infection, since many cell types can be infected with HPVs in monolayer cell culture. Here, we used chemical biology approaches to reveal that cell cycle progression through mitosis is critical for HPV infection. Using infectious HPV16 particles containing the intact viral genome, G1-synchronized human keratinocytes as hosts, and early viral gene expression as a readout for infection, we learned that the recipient cell must enter M phase (mitosis) for HPV infection to take place. Late M phase inhibitors had no effect on infection, whereas G1, S, G2, and early M phase cell cycle inhibitors efficiently prevented infection. We conclude that host cells need to pass through early prophase for successful onset of transcription of the HPV encapsidated genes. These findings provide one reason why HPVs initially establish infections in the basal compartment of stratified epithelia. Only this compartment of the epithelium contains cells progressing through the cell cycle, and therefore it is only in these cells that HPVs can establish their infection. By defining a major condition for cell susceptibility to HPV infection, these results also have potentially important implications for HPV control.

Indexed as

Cell CycleProphaseAntiviral AgentsAphidicolinCell DivisionCells, CulturedCell SurvivalEtoposideGene Expression Regulation, ViralGenome, ViralHuman papillomavirus 16HumansKeratinocytesOrthomyxoviridaeTranscription, GeneticVirionAntiviral AgentsAphidicolinEtoposide

Identifiers

PMID19247434
PMCPMC2642596
OpenAlexW2074766470

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.