Evidence map›Paper›PMID 31932884›Full record

ReviewHuman genetics2020

Susceptibility to infection in early life: a growing role for human genetics.

Alessandro Borghesi, Antonio Marzollo, Alexandre Michev, Jacques Fellay

Open access · greenAbstract 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. 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 36% 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. Article
  2. Review
  3. Article
  4. Review
  5. [Recent research on gene polymorphisms and genetic susceptibility of neonatal sepsis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Review
  6. Review
  7. Neonatal CD8+ T Cells Resist Exhaustion during Chronic Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. 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

4 authors at 4 institutions in 2 countries.

Alessandro BorghesiNeonatal Intensive Care Unit, Fondazione IRCCS Policlinico "San Matteo", Pavia, Italy. a.borghesi@smatteo.pv.it.ORCID http://orcid.org/0000-0002-8773-9144
Antonio MarzolloPediatric Hematology-Oncology Unit, Department of Women's and Children's Health, Azienda Ospedaliera-University of Padova, Padua, Italy.ORCID http://orcid.org/0000-0003-2177-8500
Alexandre MichevDepartment of Pediatrics, Fondazione IRCCS Policlinico "San Matteo", University of Pavia, Pavia, Italy.ORCID http://orcid.org/0000-0001-5035-3400
Jacques FellaySchool of Life Sciences, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.ORCID http://orcid.org/0000-0002-8240-939X
Azienda Ospedale - Università Padova · ITÉcole Polytechnique Fédérale de Lausanne · CHPoliclinico San Matteo Fondazione · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The unique vulnerability to infection of newborns and young infants is generally explained by a constellation of differences between early-life immune responses and immune responses at later ages, often referred to as neonatal immune immaturity. This developmental view, corroborated by robust evidence, offers a plausible, population-level description of the pathogenesis of life-threatening infectious diseases during the early-life period, but provides little explanation on the wide inter-individual differences in susceptibility and resistance to specific infections during the first months of life. In this context, the role of individual human genetic variation is increasingly recognized. A life-threatening infection caused by an opportunistic pathogen in an otherwise healthy infant likely represents the first manifestation of an inborn error of immunity. Single-gene disorders may also underlie common infections in full-term infants with no comorbidities or in preterm infants. In addition, there is increasing evidence of a possible role for common genetic variation in the pathogenesis of infection in preterm infants. Over the past years, a unified theory of infectious diseases emerged, supporting a hypothetical, age-dependent general model of genetic architecture of human infectious diseases. We discuss here how the proposed genetic model can be reconciled with the widely accepted developmental view of early-life infections in humans.

Indexed as

Gene Expression Regulation, DevelopmentalGenetic Predisposition to DiseaseGenetic VariationGenesGenetic Diseases, InbornHuman GeneticsHumansInfections

Identifiers

PMID31932884
OpenAlexW2999397242

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.