Evidence map›Paper›PMID 35538614›Full record

ReviewJournal of medical virology2022

Individual genetic variability mainly of Proinflammatory cytokines, cytokine receptors, and toll-like receptors dictates pathophysiology of COVID-19 disease.

Mohammad Kazem Vakil, Yaser Mansoori, Ghaidaa Raheem Lateef Al-Awsi, Ali Hosseinipour, Samaneh Ahsant, Sedigheh Ahmadi, Mohammad Ekrahi, Zahra Montaseri, Babak Pezeshki, Poopak Mohaghegh and 6 more

Open access · greenAbstract readReview
In one paragraph

Review in Journal of medical virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  9. Development of a Novel Nested-RT-LAMP Assay for the Rapid and Accurate Coronavirus Disease-2019 Diagnosis.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025
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  18. Association of specificFrontiers in immunology · 2024
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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

16 authors at 4 institutions in 2 countries.

Mohammad Kazem VakilNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Yaser MansooriNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Ghaidaa Raheem Lateef Al-AwsiUniversity of Al-Qadisiyah, College of Science, Al Diwaniyah, Iraq.
Ali HosseinipourDepartment of Internal Medicine, Fasa University of Medical Sciences, Fasa, Iran.
Samaneh AhsantNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Sedigheh AhmadiNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Mohammad EkrahiNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Zahra MontaseriDepartment of Infectious Diseases, Fasa University of Medical Sciences, Fasa, Iran.
Babak PezeshkiNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Poopak MohagheghPediatrics Department, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran.
Mojtaba SohrabpourNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Maryam BahmanyarPediatrics Department, School of Medicine, Fasa University of Medical Sciences, Fasa, Iran.
Abdolreza DaraeiDepartment of Medical Genetics, School of Medicine, Babol University of Medical Sciences, Babol, Iran.
Tahereh Dadkhah JouybariDepartment of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Alireza TavassoliDepartment of Pathology, Fasa University of Medical Sciences, Fasa, Iran.
Abdolmajid GhasemianNoncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.ORCID 0000-0002-1243-6341
Fasa University of Medical Sciences · IRBabol University of Medical Sciences · IRTarbiat Modares University · IRUniversity of Babylon · IQ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate and acquired immunity responses are crucial for viral infection elimination. However, genetic variations in coding genes may exacerbate the inflammation or initiate devastating cytokine storms which poses severe respiratory conditions in coronavirus disease-19 (COVID-19). Host genetic variations in particular those related to the immune responses determine the patients' susceptibility and COVID-19 severity and pathophysiology. Gene polymorphisms such as single nucleotide polymorphisms (SNPs) of interferons, TNF, IL1, IL4, IL6, IL7, IL10, and IL17 predispose patients to the severe form of COVID-19 or severe acute respiratory syndrome coronavirus-2 (SARS-COV-2). These variations mainly alter the gene expression and cause a severe response by B cells, T cells, monocytes, neutrophils, and natural killer cells participating in a cytokine storm. Moreover, cytokines and chemokines SNPs are associated with the severity of COVID-19 and clinical outcomes depending on the corresponding effect. Additionally, genetic variations in genes encoding toll-like receptors (TLRs) mainly TLR3, TLR7, and TLR9 have been related to the COVID-19 severe respiratory symptoms. The specific relation of these mutations with the novel variants of concern (VOCs) infection remains to be elucidated. Genetic variations mainly within genes encoding proinflammatory cytokines, cytokine receptors, and TLRs predispose patients to COVID-19 disease severity. Understanding host immune gene variations associated with the SARS-COV-2 infection opens insights to control the pathophysiology of emerging viral infections.

Indexed as

COVID-19CytokinesReceptors, CytokineToll-Like ReceptorsCytokine Release SyndromeHumansSARS-CoV-2CytokinesReceptors, CytokineToll-Like Receptorscoronavirus disease-19cytokinesgenetic variationsimmunitytoll-like receptors

Identifiers

PMID35538614
PMCPMC9348290
OpenAlexW4280497525

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.