Evidence map›Paper›PMID 32978971›Full record

ReviewClinical and experimental immunology2020

Innate immunity during SARS-CoV-2: evasion strategies and activation trigger hypoxia and vascular damage.

S Amor, L Fernández Blanco, D Baker

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 7% 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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

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  19. Neuro-Immune Interactions in Severe COVID-19 Infection.Pathogens (Basel, Switzerland) · 2022
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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 2 institutions in 2 countries.

S AmorPathology Department, VUMC, Amsterdam UMC, Amsterdam, the Netherlands.ORCID 0000-0001-6169-9845
L Fernández BlancoPathology Department, VUMC, Amsterdam UMC, Amsterdam, the Netherlands.
D BakerBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, UK.ORCID 0000-0002-8872-8711
Queen Mary University of London · GBAmsterdam University Medical Centers · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immune sensing of viral molecular patterns is essential for development of antiviral responses. Like many viruses, SARS-CoV-2 has evolved strategies to circumvent innate immune detection, including low cytosine-phosphate-guanosine (CpG) levels in the genome, glycosylation to shield essential elements including the receptor-binding domain, RNA shielding and generation of viral proteins that actively impede anti-viral interferon responses. Together these strategies allow widespread infection and increased viral load. Despite the efforts of immune subversion, SARS-CoV-2 infection activates innate immune pathways inducing a robust type I/III interferon response, production of proinflammatory cytokines and recruitment of neutrophils and myeloid cells. This may induce hyperinflammation or, alternatively, effectively recruit adaptive immune responses that help clear the infection and prevent reinfection. The dysregulation of the renin-angiotensin system due to down-regulation of angiotensin-converting enzyme 2, the receptor for SARS-CoV-2, together with the activation of type I/III interferon response, and inflammasome response converge to promote free radical production and oxidative stress. This exacerbates tissue damage in the respiratory system, but also leads to widespread activation of coagulation pathways leading to thrombosis. Here, we review the current knowledge of the role of the innate immune response following SARS-CoV-2 infection, much of which is based on the knowledge from SARS-CoV and other coronaviruses. Understanding how the virus subverts the initial immune response and how an aberrant innate immune response contributes to the respiratory and vascular damage in COVID-19 may help to explain factors that contribute to the variety of clinical manifestations and outcome of SARS-CoV-2 infection.

Indexed as

Angiotensin-Converting Enzyme 2AnimalsBetacoronavirusBlood CoagulationCoronavirus InfectionsCOVID-19HumansHypoxiaImmune EvasionImmunity, InnateInterferon Type IPandemicsPeptidyl-Dipeptidase APneumonia, ViralRenin-Angiotensin SystemSARS-CoV-2ACE2 protein, humanAngiotensin-Converting Enzyme 2Interferon Type IPeptidyl-Dipeptidase ACOVID-19endotheliaimmunologyinflammationSARS-CoV-2

Identifiers

PMID32978971
PMCPMC7537271
OpenAlexW3089111414

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.