Evidence map›Paper›PMID 25225245›Full record

ArticleInfection and immunity2014

Antigenic variation of TprK facilitates development of secondary syphilis.

Tara B Reid, Barbara J Molini, Mark C Fernandez, Sheila A Lukehart

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 47 citations in OpenAlex.

  1. The Global Syphilis Epidemic: Turning the Tide.Sexually transmitted diseases · 2026
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  13. Yaws recurrence in children at continued risk of infection.PLoS neglected tropical diseases · 2022
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  16. High-throughput nanopore sequencing ofFrontiers in microbiology · 2022
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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

4 authors at 1 institution in 1 country.

Tara B ReidInterdisciplinary Graduate Program in Pathobiology, Department of Global Health, University of Washington, Seattle, Washington, USA.
Barbara J MoliniDepartment of Medicine, University of Washington, Seattle, Washington, USA.
Mark C FernandezDepartment of Medicine, University of Washington, Seattle, Washington, USA.
Sheila A LukehartInterdisciplinary Graduate Program in Pathobiology, Department of Global Health, University of Washington, Seattle, Washington, USA Department of Medicine, University of Washington, Seattle, Washington, USA lukehart@uw.edu.
University of Washington · US

Funding

University of Washington Medical Scientist Training Program: MD/PhDT32GM007266 · NIGMS · UNIVERSITY OF WASHINGTON · PI HORWITZ, MARSHALL S. · 1985 to 2023
$30.4M
VENEREAL DISEASET32AI007140 · NIAID · UNIVERSITY OF WASHINGTON · PI Julia Cook Dombrowski · 1985 to 2026
$19.4M
TREPONEMA PALLIDUM PATHOGENESIS ASSOCIATED MOLECULESR01AI042143 · NIAID · UNIVERSITY OF WASHINGTON · PI LUKEHART, SHEILA A. · 1998 to 2015
$5.4M
Project 4: Antigenic variation of TprKR01AI063940 · NIAID · UNIVERSITY OF WASHINGTON · PI LUKEHART, SHEILA A. · 2004 to 2013
$3.3M
NIAID NIH HHS R01 AI042143NIAID NIH HHS R01AI042143NIAID NIH HHS R01 AI063940NIAID NIH HHS R01AI063940NIAID NIH HHS T32 AI007140NIAID NIH HHS T32AI007140NIGMS NIH HHS T32 GM007266NIGMS NIH HHS T32GM007266
6 · The paper itself

Abstract

Although primary syphilis lesions heal spontaneously, the infection is chronic, with subsequent clinical stages. Healing of the primary chancre occurs as antibodies against outer membrane antigens facilitate opsonophagocytosis of the bacteria by activated macrophages. TprK is an outer membrane protein that undergoes antigenic variation at 7 variable regions, and variants are selected by immune pressure. We hypothesized that individual TprK variants escape immune clearance and seed new disseminated lesions to cause secondary syphilis. As in human syphilis, infected rabbits may develop disseminated secondary skin lesions. This study explores the nature of secondary syphilis, specifically, the contribution of antigenic variation to the development of secondary lesions. Our data from the rabbit model show that the odds of secondary lesions containing predominately TprK variant treponemes is 3.3 times higher than the odds of finding TprK variants in disseminated primary lesions (odds ratio [OR] = 3.3 [95% confidence interval {CI}, 0.98 to 11.0]; P = 0.055) and that 96% of TprK variant secondary lesions are likely seeded by single treponemes. Analysis of antibody responses demonstrates significantly higher antibody titers to tprK variable region sequences found in the inoculum compared to reactivity to tprK variant sequences found in newly arising secondary lesions. This suggests that tprK variants escape the initial immune response raised against the V regions expressed in the inoculum. These data further support a role for TprK in immune evasion and suggest that the ability of TprK variants to persist despite a robust immune response is instrumental in the development of later stages of syphilis.

Indexed as

Antigenic VariationAnimalsAntibodies, BacterialBacterial ProteinsDisease Models, AnimalImmune EvasionMalePorinsRabbitsSkinSyphilisTreponema pallidumAntibodies, BacterialBacterial Proteinsmajor outer sheath protein, TreponemaPorins

Identifiers

PMID25225245
PMCPMC4249288
OpenAlexW2137787681

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.