Evidence map›Paper›PMID 33047883›Full record

ArticleImmunity, inflammation and disease2020

Association between HLA gene polymorphisms and mortality of COVID-19: An in silico analysis.

Yusuke Tomita, Tokunori Ikeda, Ryo Sato, Takuro Sakagami

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 6% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
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  11. Narrative Review Explaining the Role ofInfectious disease reports · 2024
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  15. Association of human leukocyte antigen class I and class II alleles and haplotypes in COVID-19 infection in a western Indian population.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2023
    Article
  16. The immunogenetics of COVID-19.Immunogenetics · 2023
    Review
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12 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Yusuke TomitaDepartment of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-9680-7559
Tokunori IkedaLaboratory of Clinical Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto, Japan.
Ryo SatoLaboratory of Stem Cell and Neuro-Vascular Biology, Genetics and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
Takuro SakagamiDepartment of Respiratory Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Kumamoto University · JPNational Institutes of Health · USSojo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe emergence of SARS-CoV-2 has caused global public health and economic crisis. Human leukocyte antigen (HLA) is a critical component of the viral antigen presentation pathway and plays essential roles in conferring differential viral susceptibility and severity of diseases. However, the association between HLA gene polymorphisms and risk for COVID-19 has not been fully elucidated. We hypothesized that HLA genotypes might impact on the differences in morbidity and mortality of COVID-19 across countries.

methodsWe conducted in silico analyses and examined an association of HLA gene polymorphisms with prevalence and mortality of COVID-19 by using publicly available databases.

resultsWe found that a possible association between HLA-A*02:01 and an increased risk for COVID-19. HLA-A*02:01 had a relatively lower capacity to present SARS-CoV-2 antigens compared with other frequent HLA class I molecules, HLA-A*11:01 or HLA-A*24:02.

conclusionThis study suggests that individuals with HLA-A*11:01 or HLA-A*24:02 genotypes may generate efficiently T-cell-mediated antiviral responses to SARS-CoV-2 compared with HLA-A*02:01. The differences in HLA genotypes may potentially alter the course of the disease and its transmission.

Indexed as

BetacoronavirusComputer SimulationCoronavirus InfectionsCOVID-19Gene FrequencyGenetic Predisposition to DiseaseHLA-A AntigensHost-Pathogen InteractionsHumansLinear ModelsPandemicsPneumonia, ViralPolymorphism, GeneticPrevalenceSARS-CoV-2HLA-A AntigensCOVID-19human leukocyte antigenpandemicsevere acute respiratory syndrome coronavirus 2T cell

Identifiers

PMID33047883
PMCPMC7654404
OpenAlexW3092533325

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.