Evidence map›Paper›PMID 21415020›Full record

ArticleThe Journal of infectious diseases2011

Viral load in the natural history of human papillomavirus type 16 infection: a nested case-control study.

Long Fu Xi, James P Hughes, Philip E Castle, Zoe R Edelstein, Chunhui Wang, Denise A Galloway, Laura A Koutsky, Nancy B Kiviat, Mark Schiffman

Abstract read
In one paragraph

Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Role of HPV Genotype, Multiple Infections, and Viral Load on the Risk of High-Grade Cervical Neoplasia.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2019
    Article
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

9 authors.

Long Fu XiDepartment of Pathology, School of Medicine, University of Washington, Seattle, Washington, USA. longfu@u.washington.edu
James P Hughes
Philip E Castle
Zoe R Edelstein
Chunhui Wang
Denise A Galloway
Laura A Koutsky
Nancy B Kiviat
Mark Schiffman

Funding

The Statistics, Data Science, and Data Management (SDM) CoreP30MH043520 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI MILTON L WAINBERG · 2003 to 2026
$48.2M
HPV CAPSID ANTIBODIESR01AI038382 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GALLOWAY, DENISE A. · 1995 to 2020
$4.4M
Intratypic variation of oncogenic HPV types as a risk factor for cervical neoplasR01CA133569 · NCI · UNIVERSITY OF WASHINGTON · PI XI, LONG FU · 2009 to 2012
$1.7M
NCI NIH HHS CA133569NCI NIH HHS R01 CA133569NIAID NIH HHS R01 AI038382NIMH NIH HHS P30 MH043520
6 · The paper itself

Abstract

backgroundViral load may influence the course of human papillomavirus type 16 (HPV-16) infection.

methodsThis case-control study was nested within the 2-year Atypical Squamous Cells of Undetermined Significance and Low-Grade Squamous Intraepithelial Lesion Triage Study, in which women were followed semiannually for HPV and cervical intraepithelial neoplasia (CIN). Case patients (n = 62) were women diagnosed with CIN3 following HPV-16-positive detection at a follow-up visit. HPV-16-positive controls (n = 152) without CIN2 or CIN3 were matched to cases based on the follow-up visit in which viral load was measured. Real-time polymerase chain reaction was used for HPV-16 DNA quantification.

resultsThe risk of CIN3 increased with increasing HPV-16 DNA load at the follow-up visit (odds ratio, 1.63; 95% confidence interval, 1.33-1.99 per 1 log(10) unit increase); the association was not affected by whether HPV-16 was present at enrollment. When HPV-16 was present at both enrollment and follow-up, viral load remained high among cases (P = .77) but decreased substantially among controls (P = .004). Among women with HPV-16 found initially during follow-up, viral load in the first HPV-16-positive sample was associated with short-term persistence; load was higher in those with infection, compared with those without infection, 1 visit after the initial positivity (P = .001).

conclusionsViral load of newly detected infections and changes in viral load predict persistence and progression of HPV-16 infections.

Indexed as

Human papillomavirus 16Viral LoadAdolescentAdultCase-Control StudiesDNA, ViralFemaleHumansLongitudinal StudiesOdds RatioPapillomavirus InfectionsUterine Cervical DysplasiaUterine Cervical NeoplasmsYoung AdultDNA, Viral

Identifiers

PMID21415020
PMCPMC3080901

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.