Evidence map›Paper›PMID 32918943›Full record

SynthesisVirus research2020

The role of host genetics in susceptibility to severe viral infections in humans and insights into host genetics of severe COVID-19: A systematic review.

Abdelazeem Elhabyan, Saja Elyaacoub, Ehab Sanad, Abdelwahab Abukhadra, Asmaa Elhabyan, Valentin Dinu

Open access · greenAbstract readSystematic Review
In one paragraph

Synthesis in Virus research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 3 pooled it
1.8field-weighted citation impact, top 8% 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

59 citing papers in PubMed, 3 syntheses or guidelines pooled it, 92 citations in OpenAlex.

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  9. Association ofHeliyon · 2024
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  11. Severity of oxidative stress as a hallmark in COVID-19 patients.European journal of medical research · 2023
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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

6 authors at 2 institutions in 2 countries.

Abdelazeem ElhabyanCollege of Health Solutions, Arizona State University, Scottsdale, AZ, USA; Faculty of Medicine, Tanta University, Gharbia, Tanta, Egypt. Electronic address: aelhabya@asu.edu.
Saja ElyaacoubCollege of Health Solutions, Arizona State University, Scottsdale, AZ, USA.
Ehab SanadFaculty of Medicine, Tanta University, Gharbia, Tanta, Egypt.
Abdelwahab AbukhadraFaculty of Medicine, Tanta University, Gharbia, Tanta, Egypt.
Asmaa ElhabyanFaculty of Medicine, Tanta University, Gharbia, Tanta, Egypt.
Valentin DinuCollege of Health Solutions, Arizona State University, Scottsdale, AZ, USA.
Tanta University · EGArizona State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSusceptibility to severe viral infections was reported to be associated with genetic variants in immune response genes using case reports and GWAS studies. SARS-CoV-2 is an emergent viral disease that caused millions of COVID-19 cases all over the world. Around 15 % of cases are severe and some of them are accompanied by dysregulated immune system and cytokine storm. There is increasing evidence that severe manifestations of COVID-19 might be attributed to human genetic variants in genes related to immune deficiency and or inflammasome activation (cytokine storm).

objectiveIdentify the candidate genes that are likely to aid in explaining severe COVID-19 and provide insights to understand the pathogenesis of severe COVID-19.

methodsIn this article, we systematically reviewed genes related to viral susceptibility that were reported in human genetic studies (Case-reports and GWAS) to understand the role of host viral interactions and to provide insights into the pathogenesis of severe COVID-19.

resultsWe found 40 genes associated with viral susceptibility and 21 of them were associated with severe SARS-CoV disease and severe COVID-19. Some of those genes were implicated in TLR pathways, others in C-lectin pathways, and others were related to inflammasome activation (cytokine storm).

conclusionThis compilation represents a list of candidate genes that are likely to aid in explaining severe COVID-19 which are worthy of inclusion in gene panels and during meta-analysis of different variants in host genetics studies of COVID-19. In addition, we provide several hypotheses for severe COVID-19 and possible therapeutic targets.

Indexed as

BetacoronavirusPandemicsAdolescentAdultAge FactorsAllelesCoronavirus InfectionsCOVID-19COVID-19 Drug TreatmentGenetic Predisposition to DiseaseGenome-Wide Association StudyHost-Pathogen InteractionsHumansInflammasomesLectinsMiddle AgedInflammasomesLectinsTLR3 protein, humanToll-Like Receptor 3Toll-Like ReceptorsC-lectin pathwaysCoronavirusCOVID-19COVID-19 GWASCOVID-19 pathogenesisCytokine stormHost geneticsHost immune defensesInborn errors of immunityInflammasomeInterferonInterleukinsSARS-coronavirus 2TLR pathwayViral susceptibility

Identifiers

PMID32918943
PMCPMC7480444
OpenAlexW3084235695

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.