Evidence map›Paper›PMID 36142877›Full record

ReviewInternational journal of molecular sciences2022

Correlation between Type I Interferon Associated Factors and COVID-19 Severity.

Dóra Bencze, Tünde Fekete, Kitti Pázmándi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 23 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

3 authors at 1 institution in 1 country.

Dóra BenczeDepartment of Immunology, Faculty of Medicine, University of Debrecen, 1 Egyetem Square, H-4032 Debrecen, Hungary.
Tünde FeketeDepartment of Immunology, Faculty of Medicine, University of Debrecen, 1 Egyetem Square, H-4032 Debrecen, Hungary.
Kitti PázmándiDepartment of Immunology, Faculty of Medicine, University of Debrecen, 1 Egyetem Square, H-4032 Debrecen, Hungary.ORCID 0000-0001-7709-6707
University of Debrecen · HU

Funding

European Union and the European Regional Development Fund GINOP-2.3.2-15-2016-00050János Bolyai Research Scholarship from the Hungarian Academy of Sciences bo_122_19National Research, Development and Innovation Office NKFIH FK 128294National Research, Development and Innovation Office NKFIH PD 135193New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund ÚNKP-21-05-DE-170New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund ÚNKP-21-3-II-DE-21
6 · The paper itself

Abstract

Antiviral type I interferons (IFN) produced in the early phase of viral infections effectively inhibit viral replication, prevent virus-mediated tissue damages and promote innate and adaptive immune responses that are all essential to the successful elimination of viruses. As professional type I IFN producing cells, plasmacytoid dendritic cells (pDC) have the ability to rapidly produce waste amounts of type I IFNs. Therefore, their low frequency, dysfunction or decreased capacity to produce type I IFNs might increase the risk of severe viral infections. In accordance with that, declined pDC numbers and delayed or inadequate type I IFN responses could be observed in patients with severe coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as compared to individuals with mild or no symptoms. Thus, besides chronic diseases, all those conditions, which negatively affect the antiviral IFN responses lengthen the list of risk factors for severe COVID-19. In the current review, we would like to briefly discuss the role and dysregulation of pDC/type I IFN axis in COVID-19, and introduce those type I IFN-dependent factors, which account for an increased risk of COVID-19 severity and thus are responsible for the different magnitude of individual immune responses to SARS-CoV-2.

Indexed as

COVID-19Interferon Type IAntiviral AgentsHumansInterferonsSARS-CoV-2Virus ReplicationAntiviral AgentsInterferonsInterferon Type Iantiviral responseCOVID-19IFN signatureplasmacytoid dendritic cell 1risk factorSARS-CoV-2type I interferon

Identifiers

PMID36142877
PMCPMC9506204
OpenAlexW4296462952

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.