Evidence map›Paper›PMID 36389747›Full record

ArticleFrontiers in immunology2022

Early pathogenesis profiles across SARS-CoV-2 variants in K18-hACE2 mice revealed differential triggers of lung damages.

Zhen Qin Aw, Chee Keng Mok, Yi Hao Wong, Huixin Chen, Tze Minn Mak, Raymond T P Lin, David Chien Lye, Kai Sen Tan, Justin Jang Hann Chu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
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  4. Upregulation of inflammatory genes and pathways links obesity to severe COVID-19.Biochimica et biophysica acta. Molecular basis of disease · 2024
    Article
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

9 authors at 2 institutions in 1 country.

Zhen Qin AwBiosafety Level 3 Core Facility, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Chee Keng MokBiosafety Level 3 Core Facility, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Yi Hao WongBiosafety Level 3 Core Facility, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Huixin ChenDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Tze Minn MakNational Public Health Laboratory, National Centre for Infectious Diseases, Singapore, Singapore.
Raymond T P LinDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
David Chien LyeInfectious Disease Research and Training Office, National Centre for Infectious Diseases, Singapore, Singapore.
Kai Sen TanBiosafety Level 3 Core Facility, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Justin Jang Hann ChuBiosafety Level 3 Core Facility, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
National University of Singapore · SGNational Centre for Infectious Diseases · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The on-going COVID-19 pandemic has given rise to SARS-CoV-2 clades and variants with differing levels of symptoms and severity. To this end, we aim to systematically elucidate the changes in the pathogenesis as SARS-CoV-2 evolved from ancestral to the recent Omicron VOC, on their mechanisms (e.g. cytokine storm) resulting in tissue damage, using the established K18-hACE2 murine model. We reported that among the SARS-CoV-2 viruses tested, infection profiles were initially similar between viruses from early clades but started to differ greatly starting from VOC Delta, where the trend continues in Omicron. VOCs Delta and Omicron both accumulated a significant number of mutations, and when compared to VOCs Alpha, Beta, and earlier predecessors, showed reduced neurotropism and less apparent gene expression in cytokine storm associated pathways. They were shown to leverage on other pathways to cause tissue damage (or lack of in the case of Omicron). Our study highlighted the importance of elucidating the response profiles of individual SARS-CoV-2 iterations, as their propensity of severe infection

Indexed as

COVID-19SARS-CoV-2AnimalsCytokine Release Syndromegamma-GlobulinsLungMelphalanMicePandemicsgamma-GlobulinsK-18 conjugateMelphalancytokine stormimmune responseK18-hACE2 mice modelSARS-CoV-2variants of concern

Identifiers

PMID36389747
PMCPMC9648130
OpenAlexW4307631557

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.