Evidence map›Paper›PMID 29208707›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Recurring infection with ecologically distinct HPV types can explain high prevalence and diversity.

Sylvia L Ranjeva, Edward B Baskerville, Vanja Dukic, Luisa L Villa, Eduardo Lazcano-Ponce, Anna R Giuliano, Greg Dwyer, Sarah Cobey

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 5 institutions in 3 countries.

Sylvia L RanjevaDepartment of Ecology and Evolution, University of Chicago, Chicago, IL 60637; slr@uchicago.edu.
Edward B BaskervilleDepartment of Ecology and Evolution, University of Chicago, Chicago, IL 60637.ORCID 0000-0003-4124-6472
Vanja DukicDepartment of Applied Mathematics, University of Colorado, Boulder, CO 80309.
Luisa L VillaFaculdade de Medicina, Universidade de São Paulo Department of Radiology and Oncology, Centro de Investigação Translacional em Oncologia, Universidade de São Paulo, 01246-000, São Paulo, Brazil.
Eduardo Lazcano-PonceCentro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Cuernavaca, 62100, Mexico.
Anna R GiulianoCenter for Infection Research in Cancer, Moffitt Cancer Center & Research Institute, Tampa, FL 33612.
Greg DwyerDepartment of Ecology and Evolution, University of Chicago, Chicago, IL 60637.
Sarah CobeyDepartment of Ecology and Evolution, University of Chicago, Chicago, IL 60637.
University of Chicago · USInstituto Nacional de Salud Pública · MXMoffitt Cancer Center · USUniversidade de São Paulo · BRUniversity of Colorado Boulder · US

Funding

MEDICAL SCIENTIST TRAININGT32GM007281 · NIGMS · UNIVERSITY OF CHICAGO · PI CLARK, MARCUS RAMSAY · 1985 to 2022
$32.1M
Modeling the Dynamics of Human Papillomavirus to Inform Vaccination StrategyF30AI124636 · NIAID · UNIVERSITY OF CHICAGO · PI RANJEVA, SYLVIA · 2017 to 2019
$149k
NIAID NIH HHS F30 AI124636NIGMS NIH HHS T32 GM007281
6 · The paper itself

Abstract

The high prevalence of human papillomavirus (HPV), the most common sexually transmitted infection, arises from the coexistence of over 200 genetically distinct types. Accurately predicting the impact of vaccines that target multiple types requires understanding the factors that determine HPV diversity. The diversity of many pathogens is driven by type-specific or "homologous" immunity, which promotes the spread of variants to which hosts have little immunity. To test for homologous immunity and to identify mechanisms determining HPV transmission, we fitted nonlinear mechanistic models to longitudinal data on genital infections in unvaccinated men. Our results provide no evidence for homologous immunity, instead showing that infection with one HPV type strongly increases the risk of infection with that type for years afterward. For HPV16, the type responsible for most HPV-related cancers, an initial infection increases the 1-year probability of reinfection by 20-fold, and the probability of reinfection remains 14-fold higher 2 years later. This increased risk occurs in both sexually active and celibate men, suggesting that it arises from autoinoculation, episodic reactivation of latent virus, or both. Overall, our results suggest that high HPV prevalence and diversity can be explained by a combination of a lack of homologous immunity, frequent reinfections, weak competition between types, and variation in type fitness between host subpopulations. Because of the high risk of reinfection, vaccinating boys who have not yet been exposed may be crucial to reduce prevalence, but our results suggest that there may also be large benefits to vaccinating previously infected individuals.

Indexed as

AdolescentAdultAgedAlphapapillomavirusHumansMaleMiddle AgedModels, StatisticalPapillomavirus InfectionsPrevalenceRecurrenceecologyinfectious diseasemathematical modelpublic healthvaccination

Identifiers

PMID29208707
PMCPMC5754802
OpenAlexW2773614109

What OpenQuestion holds

Textmetadata
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.