Evidence map›Paper›PMID 25569261›Full record

ArticleGenes and immunity

The genetic basis for susceptibility to Rift Valley fever disease in MBT/Pas mice.

S Tokuda, T Z Do Valle, L Batista, D Simon-Chazottes, L Guillemot, M Bouloy, M Flamand, X Montagutelli, J-J Panthier

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  4. Review
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  6. Article
  7. The ring finger protein 213 gene (Rnf213) contributes to Rift Valley fever resistance in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2021
    Article
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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

9 authors at 2 institutions in 1 country.

S Tokuda1] Institut Pasteur, Developmental & Stem Cell Biology Department, Mouse functional Genetics, Paris, France [2] Centre National de la Recherche Scientifique, URA 2578, Paris, France.
T Z Do Valle1] Institut Pasteur, Developmental & Stem Cell Biology Department, Mouse functional Genetics, Paris, France [2] Centre National de la Recherche Scientifique, URA 2578, Paris, France [3] Instituto Oswaldo Cruz, Laboratório de Imunomodulação e Protozoologia, Fiocruz, Rio de Janeiro, Brasil.
L Batista1] Institut Pasteur, Developmental & Stem Cell Biology Department, Mouse functional Genetics, Paris, France [2] Centre National de la Recherche Scientifique, URA 2578, Paris, France [3] Sorbonne Universités, UPMC Univ Paris 06, IFD, Paris, France.
D Simon-Chazottes1] Institut Pasteur, Developmental & Stem Cell Biology Department, Mouse functional Genetics, Paris, France [2] Centre National de la Recherche Scientifique, URA 2578, Paris, France.
L Guillemot1] Institut Pasteur, Developmental & Stem Cell Biology Department, Mouse functional Genetics, Paris, France [2] Centre National de la Recherche Scientifique, URA 2578, Paris, France.
M BouloyInstitut Pasteur, Bunyaviruses Molecular Genetics, Paris, France.
M FlamandInstitut Pasteur, Structural Virology, Paris, France.
X Montagutelli1] Institut Pasteur, Developmental & Stem Cell Biology Department, Mouse functional Genetics, Paris, France [2] Centre National de la Recherche Scientifique, URA 2578, Paris, France.
J-J Panthier1] Institut Pasteur, Developmental & Stem Cell Biology Department, Mouse functional Genetics, Paris, France [2] Centre National de la Recherche Scientifique, URA 2578, Paris, France.
Institut Pasteur · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The large variation in individual response to infection with Rift Valley fever virus (RVFV) suggests that host genetic determinants play a role in determining virus-induced disease outcomes. These genetic factors are still unknown. The systemic inoculation of mice with RVFV reproduces major pathological features of severe human disease, notably the hepatitis and encephalitis. A genome scan performed on 546 (BALB/c × MBT) F2 progeny identified three quantitative trait loci (QTLs), denoted Rvfs-1 to Rvfs-3, that were associated with disease susceptibility in MBT/Pas mice. Non-parametric interval-mapping revealed one significant and two suggestive linkages with survival time on chromosomes 2 (Rvfs-1), 5 (Rvfs-3) and 11 (Rvfs-2) with respective logarithm of odds (LOD) scores of 4.58, 2.95 and 2.99. The two-part model, combining survival time and survival/death, identified one significant linkage to Rvfs-2 and one suggestive linkage to Rvfs-1 with respective LOD scores of 5.12 and 4.55. Under a multiple model, with additive effects and sex as a covariate, the three QTLs explained 8.3% of the phenotypic variance. Sex had the strongest influence on susceptibility. The contribution of Rvfs-1, Rvfs-2 and Rvfs-3 to survival time of RVFV-infected mice was further confirmed in congenic mice.

Indexed as

Genetic Predisposition to DiseaseRift Valley fever virusAnimalsDisease Models, AnimalDisease SusceptibilityFemaleGenetic MarkersGenome-Wide Association StudyHaplotypesLod ScoreMaleMicePhenotypePolymorphism, GeneticQuantitative Trait LociRift Valley FeverGenetic Markers

Identifiers

PMID25569261
OpenAlexW2034996193

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.