Evidence map›Paper›PMID 32277285›Full record

ReviewHuman genetics2020

Genetic algorithms identify individuals with high risk of severe liver disease caused by schistosomes.

Hélia Dessein, Nicolas Duflot, Audrey Romano, Christopher Opio, Valeria Pereira, Carla Mola, Narcis Kabaterene, Ana Coutinho, Alain Dessein

Erratum issuedAbstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Pathogens (Basel, Switzerland) · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Cellular Mechanisms of Liver Fibrosis.Frontiers in pharmacology · 2021
    Review
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 3 countries.

Hélia DesseinBILHI Genetics, 60 Avenue André Roussin, 13016, Marseille, France.
Nicolas DuflotBILHI Genetics, 60 Avenue André Roussin, 13016, Marseille, France.
Audrey RomanoBILHI Genetics, 60 Avenue André Roussin, 13016, Marseille, France.
Christopher OpioDepartment of Medicine, Mulago Hospital, Makerere University College of Health Sciences, Kampala, Uganda.
Valeria PereiraInstituto Aggeu Magalhães, Fiocruz, Fundaçao Oswaldo Cruz, Av. Professor Moraes Rego, S/N Cidade Universitária, Recife, PE, 50740-465, Brazil.
Carla MolaInstituto Aggeu Magalhães, Fiocruz, Fundaçao Oswaldo Cruz, Av. Professor Moraes Rego, S/N Cidade Universitária, Recife, PE, 50740-465, Brazil.
Narcis KabatereneVector Control Division Uganda, Ministry of Health, Queen's Ln, Kampala, Uganda.
Ana CoutinhoFundação Oswaldo Cruz Rio de Janeiro, Av. Brasil, 4365, Rio de Janeiro, RJ, 21040-360, Brazil.
Alain DesseinBILHI Genetics, 60 Avenue André Roussin, 13016, Marseille, France. alain.dessein@bilhigenetics.com.ORCID http://orcid.org/0000-0001-5339-2456
Inserm · FRFundação Oswaldo Cruz · BRMinistry of Health · UGMulago Hospital · UG

Funding

INSERM U906
6 · The paper itself

Abstract

Schistosomes induce severe hepatic disease, which is fatal in 2-10% of cases, mortality being higher in cases of co-infection with HBV or HCV. Hepatic disease occurs as a consequence of the chronic inflammation caused by schistosome eggs trapped in liver sinusoids. In certain individuals, the repair process leads to a massive accumulation of fibrosis in the periportal spaces. We and others have shown that genetic variants play a crucial role in disease progression from mild to severe fibrosis and explain why hepatic fibrosis progresses rapidly in certain subjects only. We will review here published findings concerning the strategies that have been used in the analysis of hepatic fibrosis in schistosome-infected individuals, the genetic variants that have associated with fibrosis, and variants in new pathways crucial for fibrosis progression. Together, these studies show that the development of fibrosis is under the tight genetic control of various common variants with moderate effects. This polygenic control has made it possible to develop models that identify schistosome-infected individual at risk of severe hepatic disease. We discuss the performances and limitations of these models.

Indexed as

AlgorithmsGenetic MarkersPrecision MedicineSeverity of Illness IndexAnimalsDisease ProgressionHumansLiver Diseases, ParasiticSchistosomaSchistosomiasisGenetic Markers

Identifiers

PMID32277285
OpenAlexW3015725732

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.