Evidence map›Paper›PMID 10768966›Full record

ArticleInfection and immunity2000

Heterologous expression of Trypanosoma cruzi trans-sialidase in Leishmania major enhances virulence.

M Belen Carrillo, W Gao, M Herrera, J Alroy, J B Moore, S M Beverley, M A Pereira

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 41 citations in OpenAlex.

  1. Use ofFrontiers in microbiology · 2022
    Article
  2. Major Molecular Factors Related toFrontiers in immunology · 2022
    Review
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  16. Thymocyte depletion in Trypanosoma cruzi infection is mediated by trans-sialidase-induced apoptosis on nurse cells complex.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  17. Article
  18. Article
  19. 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

7 authors at 4 institutions in 1 country.

M Belen CarrilloParasitology Research Center, Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
W Gao
M Herrera
J Alroy
J B Moore
S M Beverley
M A Pereira
Tufts University · USHarvard University · USTufts Medical Center · USWashington University in St. Louis · US

Funding

MOLECULAR GENETICS OF LEISHMANIA USING DNA TRANSFECTIONR01AI029646 · NIAID · WASHINGTON UNIVERSITY · PI BEVERLEY, STEPHEN M · 1990 to 2015
$9.3M
SURFACE RECEPTORS IN TRYPANOSOMA CRUZIR01AI018102 · NIAID · TUFTS UNIVERSITY BOSTON · PI PEREIRAPERRIN, MERCIO A · 1985 to 1985
–
NIAID NIH HHS AI 18102NIAID NIH HHS AI 29646NIAID NIH HHS R01 AI029646
6 · The paper itself

Abstract

Earlier studies showed that mice primed for a few hours with the trans-sialidase (TS) of Trypanosoma cruzi, the agent of Chagas' disease, become highly susceptible to trypanosomal infection. These studies suggest that TS affects parasite virulence independent of antigenic stimulation. Potentially, TS could enhance or reduce the virulence of heterologous microbes depending on the mechanism of TS action and on the type of immune response elicited by the particular parasite. We tested this hypothesis by expressing heterologous TS in Leishmania major, a protozoan parasite that causes cutaneous leishmaniasis and lacks TS and the TS product alpha2-3-linked sialic acid. Leishmania cells transfected with a T. cruzi TS expression construct made high levels of active enzyme, which was present in the promastigotes and shed into the extracellular milieu. TS expression did not affect L. major binding to and entry into cultured macrophages or its tropism for macrophage infection in vivo. However, TS-expressing L. major exhibited elevated virulence in BALB/c mice, as determined by lesion progression, parasite numbers, and macro- and microscopic examination of cutaneous lesions. Several genetic tests proved that the enhanced virulence was directly attributable to TS expression. The results are consistent with TS functioning to sabotage the mouse immune system to confer a growth advantage on T. cruzi and transgenic L. major. These data suggest that heterologous expression of T. cruzi virulence factors in Leishmania may provide a new approach for dissecting their function in vivo.

Indexed as

AnimalsDisease Models, AnimalFemaleGene ExpressionGlycoproteinsLeishmania majorLeishmaniasis, CutaneousMiceMice, Inbred BALB CMice, Inbred C57BLNeuraminidaseTrypanosoma cruziVirulenceGlycoproteinsNeuraminidasetrans-sialidase

Identifiers

PMID10768966
PMCPMC97481
OpenAlexW2143399059

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.