Evidence map›Paper›PMID 33872774›Full record

ReviewEuropean journal of medical genetics2021

Why does SARS-CoV-2 hit in different ways? Host genetic factors can influence the acquisition or the course of COVID-19.

Maria Monticelli, Bruno Hay Mele, Giuseppina Andreotti, Maria Vittoria Cubellis, Guglielmo Riccio

Open access · greenAbstract readReview
In one paragraph

Review in European journal of medical genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  12. Investigation ofPathogens and global health · 2022
    Article
  13. Article
  14. Review
  15. Frontiers in immunology · 2022
    Article
  16. Potential Genes Associated with COVID-19 and Comorbidity.International journal of medical sciences · 2022
    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

5 authors at 4 institutions in 1 country.

Maria MonticelliDepartment of Biology, Università Federico II, 80126, Napoli, Italy. Electronic address: maria.monticelli@unina.it.
Bruno Hay MeleIntegrative Marine Ecology Department, Stazione Zoologica Anton Dohrn, Villa Comunale, 80121, Napoli, Italy. Electronic address: bruno.haymele@szn.it.
Giuseppina AndreottiIstituto di Chimica Biomolecolare -CNR, 80078, Pozzuoli, Italy. Electronic address: gandreotti@icb.cnr.it.
Maria Vittoria CubellisDepartment of Biology, Università Federico II, 80126, Napoli, Italy; Istituto di Chimica Biomolecolare -CNR, 80078, Pozzuoli, Italy. Electronic address: cubellis@unina.it.
Guglielmo RiccioScuola di Specializzazione in Pediatria, Università degli Studi di Trieste, 34127, Trieste, Italy. Electronic address: gugli.riccio@libero.it.
Istituto di Chimica Biomolecolare · ITStazione Zoologica Anton Dohrn · ITUniversity of Naples Federico II · ITUniversity of Trieste · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The identification of high-risk factors for the infection by SARS-CoV-2 and the negative outcome of COVID-19 is crucial. The genetic background of the host might account for individual responses to SARS-CoV-2 infection besides age and comorbidities. A list of candidate polymorphisms is needed to drive targeted screens, given the existence of frequent polymorphisms in the general population. We carried out text mining in the scientific literature to draw up a list of genes referable to the term "SARS-CoV*". We looked for frequent mutations that are likely to affect protein function in these genes. Ten genes, mostly involved in innate immunity, and thirteen common variants were identified, for some of these the involvement in COVID-19 is supported by publicly available epidemiological data. We looked for available data on the population distribution of these variants and we demonstrated that the prevalence of five of them, Arg52Cys (rs5030737), Gly54Asp (rs1800450) and Gly57Glu (rs1800451) in MBL2, Ala59Thr (rs25680) in CD27, and Val197Met (rs12329760) in TMPRSS2, correlates with the number of cases and/or deaths of COVID-19 observed in different countries. The association of the TMPRSS2 variant provides epidemiological evidence of the usefulness of transmembrane protease serine 2 inhibitors for the cure of COVID-19. The identified genetic variants represent a basis for the design of a cost-effective assay for population screening of genetic risk factors in the COVID-19 pandemic.

Indexed as

Genetic Predisposition to DiseaseImmunity, InnateCOVID-19Data MiningGene FrequencyGenetic VariationHost Microbial InteractionsHumansMannose-Binding LectinPolymorphism, Single NucleotideRisk FactorsSARS-CoV-2Serine EndopeptidasesTumor Necrosis Factor Receptor Superfamily, Member 7Mannose-Binding LectinMBL2 protein, humanSerine EndopeptidasesTMPRSS2 protein, humanTumor Necrosis Factor Receptor Superfamily, Member 7CD27COVID19Data miningMBL2SNPsTMPRSS2

Identifiers

PMID33872774
PMCPMC8051015
OpenAlexW3155889931

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.