Evidence map›Paper›PMID 38286985›Full record

ArticleCell death & disease2024

Necroptosis does not drive disease pathogenesis in a mouse infective model of SARS-CoV-2 in vivo.

Stefanie M Bader, James P Cooney, Reet Bhandari, Liana Mackiewicz, Merle Dayton, Dylan Sheerin, Smitha Rose Georgy, James M Murphy, Kathryn C Davidson, Cody C Allison and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.1field-weighted citation impact, top 8% 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, 13 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Stefanie M BaderThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.ORCID 0000-0002-7901-9833
James P CooneyThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Reet BhandariThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Liana MackiewiczThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Merle DaytonThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Dylan SheerinThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Smitha Rose GeorgyDepartment of Anatomic Pathology, Faculty of Veterinary and Agricultural Sciences, University of Melbourne, Werribee, VIC, 3030, Australia.
James M MurphyThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.ORCID 0000-0003-0195-3949
Kathryn C DavidsonThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Cody C AllisonThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Marc Pellegrini *The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.ORCID 0000-0003-3627-3126
Marcel Doerflinger *The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia. doerflinger.m@wehi.edu.au.ORCID 0000-0001-9159-3021
The University of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

Department of Health | National Health and Medical Research Council (NHMRC) GNT1172929Department of Health | National Health and Medical Research Council (NHMRC) GNT1175011
6 · The paper itself

Abstract

Necroptosis, a type of lytic cell death executed by the pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) has been implicated in the detrimental inflammation caused by SARS-CoV-2 infection. We minimally and extensively passaged a single clinical SARS-CoV-2 isolate to create models of mild and severe disease in mice allowing us to dissect the role of necroptosis in SARS-CoV-2 disease pathogenesis. We infected wild-type and MLKL-deficient mice and found no significant differences in viral loads or lung pathology. In our model of severe COVID-19, MLKL-deficiency did not alter the host response, ameliorate weight loss, diminish systemic pro-inflammatory cytokines levels, or prevent lethality in aged animals. Our in vivo models indicate that necroptosis is dispensable in the pathogenesis of mild and severe COVID-19.

Indexed as

COVID-19SARS-CoV-2AnimalsDisease Models, AnimalMiceNecroptosisProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesProtein KinasesReceptor-Interacting Protein Serine-Threonine Kinases

Identifiers

PMID38286985
PMCPMC10825138
OpenAlexW4391328340

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.