Evidence map›Paper›PMID 35618037›Full record

ReviewEuropean journal of pharmacology2022

Type-I interferons in the immunopathogenesis and treatment of Coronavirus disease 2019.

Hossein Khorramdelazad, Mohammad Hossein Kazemi, Maryam Azimi, Azin Aghamajidi, Ali Zarezadeh Mehrabadi, Faezeh Shahba, Nazanin Aghamohammadi, Reza Falak, Fatemeh Faraji, Reza Jafari

Open access · greenAbstract readReview
In one paragraph

Review in European journal of pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Article
  6. Review
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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

10 authors at 2 institutions in 1 country.

Hossein KhorramdelazadDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: H.khoramdel@rums.ac.ir.
Mohammad Hossein KazemiDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Kazemi.m03@iums.ac.ir.
Maryam AzimiImmunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Azimi.mr@iums.ac.ir.
Azin AghamajidiDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Aghamajidi.a@iums.ac.ir.
Ali Zarezadeh MehrabadiDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Zarezade.a@iums.ac.ir.
Faezeh ShahbaDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Shahba.f@iums.ac.ir.
Nazanin AghamohammadiDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Aghamohammadi.n@iums.ac.ir.
Reza FalakDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran; Immunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Falak.r@iums.ac.ir.
Fatemeh FarajiImmunology Research Center, Institute of Immunology and Infectious Diseases, Iran University of Medical Sciences, Tehran, Iran. Electronic address: Faraji.fat@iums.ac.ir.
Reza JafariCellular and Molecular Research Center, Cellular and Molecular Medicine Institute, Urmia University of Medical Sciences, Urmia, Iran. Electronic address: Jafari.reza@umsu.ac.ir.
Iran University of Medical Sciences · IRUrmia University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is currently the major global health problem. Still, it continues to infect people globally and up to the end of February 2022, over 436 million confirmed cases of COVID-19, including 5.95 million deaths, were reported to the world health organization (WHO). No specific treatment is currently available for COVID-19, and the discovery of effective therapeutics requires understanding the effective immunologic and immunopathologic mechanisms behind this infection. Type-I interferons (IFN-Is), as the critical elements of the immediate immune response against viral infections, can inhibit the replication and spread of the viruses. However, the available evidence shows that the antiviral IFN-I response is impaired in patients with the severe form of COVID-19. Moreover, the administration of exogenous IFN-I in different phases of the disease can lead to various outcomes. Therefore, understanding the role of IFN-I molecules in COVID-19 development and its severity can provide valuable information for better management of this disease. This review summarizes the role of IFN-Is in the pathogenesis of COIVD-19 and discusses the importance of autoantibodies against this cytokine in the spreading of SARS-CoV-2 and control of the subsequent excessive inflammation.

Indexed as

COVID-19 Drug TreatmentInterferon Type ICytokinesHumansSARS-CoV-2CytokinesInterferon Type IAutoantibodyCOVID-19ImmunopathogenesisInflammationSARS-CoV-2Type-I interferons

Identifiers

PMID35618037
PMCPMC9124632
OpenAlexW4281286110

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.