Evidence map›Paper›PMID 36934789›Full record

ReviewInfection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases2023

Genetic susceptibility to severe COVID-19.

Claudio Cappadona, Valeria Rimoldi, Elvezia Maria Paraboschi, Rosanna Asselta

Open access · goldAbstract readReview
In one paragraph

Review in Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Claudio CappadonaDepartment of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, Pieve Emanuele - Milan 20072, Italy.
Valeria RimoldiDepartment of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, Pieve Emanuele - Milan 20072, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, Rozzano, Milan 20089, Italy.
Elvezia Maria ParaboschiDepartment of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, Pieve Emanuele - Milan 20072, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, Rozzano, Milan 20089, Italy.
Rosanna AsseltaDepartment of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini 4, Pieve Emanuele - Milan 20072, Italy; IRCCS Humanitas Research Hospital, Via Manzoni 56, Rozzano, Milan 20089, Italy. Electronic address: rosanna.asselta@hunimed.eu.
Humanitas University · ITIRCCS Humanitas Research Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent of the coronavirus disease 2019 (COVID-19) pandemic. Clinical manifestations of the disease range from an asymptomatic condition to life-threatening events and death, with more severe courses being associated with age, male sex, and comorbidities. Besides these risk factors, intrinsic characteristics of the virus as well as genetic factors of the host are expected to account for COVID-19 clinical heterogeneity. Genetic studies have long been recognized as fundamental to identify biological mechanisms underlying congenital diseases, to pinpoint genes/proteins responsible for the susceptibility to different inherited conditions, to highlight targets of therapeutic relevance, to suggest drug repurposing, and even to clarify causal relationships that make modifiable some environmental risk factors. Though these studies usually take long time to be concluded and, above all, to translate their discoveries to patients' bedside, the scientific community moved really fast to deliver genetic signals underlying different COVID-19 phenotypes. In this Review, besides a concise description of COVID-19 symptomatology and of SARS-CoV-2 mechanism of infection, we aimed to recapitulate the current literature in terms of host genetic factors that specifically associate with an increased severity of the disease.

Indexed as

COVID-19ComorbidityGenetic Predisposition to DiseaseHumansMaleRisk FactorsSARS-CoV-2COVID-19GeneticsGenome-wide association studyMutationSARS-CoV-2Severity

Identifiers

PMID36934789
PMCPMC10022467
OpenAlexW4327703856

What Socratic 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 Socratic graph.