Evidence map›Paper›PMID 32962761›Full record

SynthesisAdvances in rheumatology (London, England)2020

Severe COVID-19: what have we learned with the immunopathogenesis?

Bruno Bordallo, Mozart Bellas, Arthur Fernandes Cortez, Matheus Vieira, Marcelo Pinheiro

Abstract readSystematic Review
In one paragraph

Synthesis in Advances in rheumatology (London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

45 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Review
  8. Meeting the Challenge of Controlling Viral Immunopathology.International journal of molecular sciences · 2024
    Review
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  13. 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

5 authors.

Bruno BordalloDepartament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Univesidade Federal Fluminense, Niterói, RJ, Brazil. brunobaf@hotmail.com.ORCID 0000-0003-1336-4439
Mozart BellasDepartament of Internal Medicine / Emergence, Hospital Universitário Antônio Pedro / Universidade Federal Fluminense, Niterói, RJ, Brazil.
Arthur Fernandes CortezHospital Universitário Gaffré e Guinle / Universidade Federal do Estado do Rio de Janeiro, Internal Medicine Departament, Rio de Janeiro, RJ, Brazil.
Matheus VieiraDepartament of Internal Medicine, Hospital Universitário Clementino Fraga Filho, Rio de Janeiro, RJ, Brazil.
Marcelo PinheiroDepartament of Rheumatology, Universidade Federal de São Paulo, Sao Paulo, SP, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global major concern. In this review, we addressed a theoretical model on immunopathogenesis associated with severe COVID-19, based on the current literature of SARS-CoV-2 and other epidemic pathogenic coronaviruses, such as SARS and MERS. Several studies have suggested that immune dysregulation and hyperinflammatory response induced by SARS-CoV-2 are more involved in disease severity than the virus itself.Immune dysregulation due to COVID-19 is characterized by delayed and impaired interferon response, lymphocyte exhaustion and cytokine storm that ultimately lead to diffuse lung tissue damage and posterior thrombotic phenomena.Considering there is a lack of clinical evidence provided by randomized clinical trials, the knowledge about SARS-CoV-2 disease pathogenesis and immune response is a cornerstone to develop rationale-based clinical therapeutic strategies. In this narrative review, the authors aimed to describe the immunopathogenesis of severe forms of COVID-19.

Indexed as

Age FactorsAngiotensin-Converting Enzyme 2AnimalsAntibody FormationBetacoronavirusBlood Coagulation DisordersComorbidityCoronavirus InfectionsCOVID-19Cytokine Release SyndromeHumansImmunity, InnateInflammationLungLymphopeniaMiceACE2 protein, humanAce2 protein, mouseAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase ACOVID-19CytokineCytokine stormImmunologyInflammationMacrophage activation syndromeSARS-CoV-2Thrombosis

Identifiers

PMID32962761
PMCPMC7506814

What OpenQuestion holds

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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.