Evidence map›Paper›PMID 37187043›Full record

ReviewImmunobiology2023

Complement and COVID-19: Three years on, what we know, what we don't know, and what we ought to know.

Wioleta M Zelek, Richard A Harrison

Open access · hybridAbstract readReview
In one paragraph

Review in Immunobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Review
  7. Article
  8. Article
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  15. Article
  16. Epidemiological Study in Antiviral Innate Immunity.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. Immunity and Coagulation in COVID-19.International journal of molecular sciences · 2024
    Review
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

2 authors at 2 institutions in 1 country.

Wioleta M ZelekDementia Research Institute and Division of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, United Kingdom.
Richard A HarrisonSchool of Medicine, Cardiff University, Cardiff, United Kingdom. Electronic address: harrisonR4@cardiff.ac.uk.
Cardiff University · GBUK Dementia Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus was identified in China in 2019 as the causative agent of COVID-19, and quickly spread throughout the world, causing over 7 million deaths, of which 2 million occurred prior to the introduction of the first vaccine. In the following discussion, while recognising that complement is just one of many players in COVID-19, we focus on the relationship between complement and COVID-19 disease, with limited digression into directly-related areas such as the relationship between complement, kinin release, and coagulation. Prior to the 2019 COVID-19 outbreak, an important role for complement in coronavirus diseases had been established. Subsequently, multiple investigations of patients with COVID-19 confirmed that complement dysregulation is likely to be a major driver of disease pathology, in some, if not all, patients. These data fuelled evaluation of many complement-directed therapeutic agents in small patient cohorts, with claims of significant beneficial effect. As yet, these early results have not been reflected in larger clinical trials, posing questions such as who to treat, appropriate time to treat, duration of treatment, and optimal target for treatment. While significant control of the pandemic has been achieved through a global scientific and medical effort to comprehend the etiology of the disease, through extensive SARS-CoV-2 testing and quarantine measures, through vaccine development, and through improved therapy, possibly aided by attenuation of the dominant strains, it is not yet over. In this review, we summarise complement-relevant literature, emphasise its main conclusions, and formulate a hypothesis for complement involvement in COVID-19. Based on this we make suggestions as to how any future outbreak might be better managed in order to minimise impact on patients.

Indexed as

COVID-19Complement System ProteinsCOVID-19 TestingHumansPandemicsSARS-CoV-2Complement System Proteins

Identifiers

PMID37187043
PMCPMC10174470
OpenAlexW4376127337

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.