Evidence map›Paper›PMID 25092910›Full record

ArticleInfection and immunity2014

A conserved apicomplexan microneme protein contributes to Toxoplasma gondii invasion and virulence.

My-Hang Huynh, Martin J Boulanger, Vern B Carruthers

Abstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–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

22 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. The CLAMP-Linked Invasion Protein (CLIP) plays an essential role inbioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Mining the Proteome ofAnimals : an open access journal from MDPI · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. The Journal of biological chemistry · 2020
    Article
  14. Article
  15. Article
  16. Recent progress in microneme-based vaccines development againstClinical and experimental vaccine research · 2018
    Review
  17. Article
  18. Immuno-Efficacy of aFrontiers in microbiology · 2017
    Article
  19. Frontiers in microbiology · 2017
    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

3 authors.

My-Hang HuynhDepartment of Microbiology and Immunology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA.
Martin J BoulangerDepartment of Biochemistry & Microbiology, University of Victoria, Victoria, British Columbia, Canada.
Vern B CarruthersDepartment of Microbiology and Immunology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA vcarruth@umich.edu.

Funding

MICRONEME FUNCTION IN TOXOPLASMAR01AI046675 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARRUTHERS, VERNON BRUCE · 2000 to 2021
$6.5M
Mediators of Toxoplasma surviral during infectionR03AI060838 · NIAID · JOHNS HOPKINS UNIVERSITY · PI CARRUTHERS, VERNON BRUCE · 2004 to 2004
$82k
CIHR MOP82915NIAID NIH HHS R01 AI046675NIAID NIH HHS R01AI046675NIAID NIH HHS R03 AI060838
6 · The paper itself

Abstract

The obligate intracellular parasite Toxoplasma gondii critically relies on host cell invasion during infection. Proteins secreted from the apical micronemes are central components for host cell recognition, invasion, egress, and virulence. Although previous work established that the sporozoite protein with an altered thrombospondin repeat (SPATR) is a micronemal protein conserved in other apicomplexan parasites, including Plasmodium, Neospora, and Eimeria, no genetic evidence of its contribution to invasion has been reported. SPATR contains a predicted epidermal growth factor domain and two thrombospondin type 1 repeats, implying a role in host cell recognition. In this study, we assess the contribution of T. gondii SPATR (TgSPATR) to T. gondii invasion by genetically ablating it and restoring its expression by genetic complementation. Δspatr parasites were ~50% reduced in invasion compared to parental strains, a defect that was reversed in the complemented strain. In mouse virulence assays, Δspatr parasites were significantly attenuated, with ~20% of mice surviving infection. Given the conservation of this protein among the Apicomplexa, we assessed whether the Plasmodium falciparum SPATR ortholog (PfSPATR) could complement the absence of the TgSPATR. Although PfSPATR showed correct micronemal localization, it did not reverse the invasion deficiency of Δspatr parasites, because of an apparent failure in secretion. Overall, the results suggest that TgSPATR contributes to invasion and virulence, findings that have implications for the many genera and life stages of apicomplexans that express SPATR.

Indexed as

AnimalsDisease Models, AnimalFemaleGene DeletionGenetic Complementation TestMiceProtozoan ProteinsSurvival AnalysisThrombospondinsToxoplasmaToxoplasmosis, AnimalVirulenceVirulence FactorsProtozoan ProteinsThrombospondinsVirulence Factors

Identifiers

PMID25092910
PMCPMC4187870

What OpenQuestion holds

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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.