Evidence map›Paper›PMID 27352043›Full record

ArticlePLoS neglected tropical diseases2016

Concomitant Immunity Induced by Persistent Leishmania major Does Not Preclude Secondary Re-Infection: Implications for Genetic Exchange, Diversity and Vaccination.

Michael A Mandell, Stephen M Beverley

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Commentary on the Issue ofVeterinary sciences · 2025
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  4. Immune response to viscerotropicFrontiers in immunology · 2024
    Review
  5. Review
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  9. Article
  10. Article
  11. Review
  12. Frontiers in cellular and infection microbiology · 2019
    Review
  13. Article
  14. Review
  15. Continual renewal and replication of persistent Leishmania major parasites in concomitantly immune hosts.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

2 authors at 1 institution in 1 country.

Michael A MandellDepartment of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Stephen M BeverleyDepartment of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri, United States of America.ORCID 0000-0001-5319-0811
Washington University in St. Louis · US

Funding

GLYCOSYLATION MUTANTS OF LEISHMANIAR01AI031078 · NIAID · WASHINGTON UNIVERSITY · PI BEVERLEY, STEPHEN M · 1992 to 2019
$11.4M
MOLECULAR GENETICS OF LEISHMANIA USING DNA TRANSFECTIONR01AI029646 · NIAID · WASHINGTON UNIVERSITY · PI BEVERLEY, STEPHEN M · 1990 to 2015
$9.3M
NIAID NIH HHS R01 AI029646NIAID NIH HHS R01 AI031078
6 · The paper itself

Abstract

backgroundMany microbes have evolved the ability to co-exist for long periods of time within other species in the absence of overt pathology. Evolutionary biologists have proposed benefits to the microbe from 'asymptomatic persistent infections', most commonly invoking increased likelihood of transmission by longer-lived hosts. Typically asymptomatic persistent infections arise from strong containment by the immune system, accompanied by protective immunity; such 'vaccination' from overt disease in the presence of a non-sterilizing immune response is termed premunition or concomitant immunity. Here we consider another potential benefit of persistence and concomitant immunity to the parasite: the 'exclusion' of competing super-infecting strains, which would favor transmission of the original infecting organism. METHODOLOGY / PRINCIPLE

findingsTo investigate this in the protozoan parasite Leishmania major, a superb model for the study of asymptomatic persistence, we used isogenic lines of comparable virulence bearing independent selectable markers. One was then used to infect genetically resistant mice, yielding infections which healed and progressed to asymptomatic persistent infection; these mice were then super-infected with the second marked line. As anticipated, super-infection yielded minimal pathology, showing that protective immunity against disease pathology had been established. The relative abundance of the primary and super-infecting secondary parasites was then assessed by plating on selective media. The data show clearly that super-infecting parasites were able to colonize the immune host effectively, achieving numbers comparable to and sometimes greater than that of the primary parasite. CONCLUSIONS / SIGNIFICANCE: We conclude that induction of protective immunity does not guarantee the Leishmania parasite exclusive occupation of the infected host. This finding has important consequences to the maintenance and generation of parasite diversity in the natural Leishmania infectious cycle alternating between mammalian and sand fly hosts.

Indexed as

Genetic Predisposition to DiseaseAnimalsFemaleGenetic VariationLeishmania majorLeishmaniasis, CutaneousMiceMice, Inbred C57BLProtozoan VaccinesRecurrenceVirulenceProtozoan Vaccines

Identifiers

PMID27352043
PMCPMC4924822
OpenAlexW2462605353

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.