Evidence map›Paper›PMID 38941138›Full record

ArticleeLife2024

Self-inhibiting percolation and viral spreading in epithelial tissue.

Xiaochan Xu, Bjarke Frost Nielsen, Kim Sneppen

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Xiaochan XuNiels Bohr Institute, University of Copenhagen, Copenhagen, Denmark.
Bjarke Frost NielsenPandemiX Center, Department of Science and Environment, Roskilde University, Roskilde, Denmark.
Kim SneppenNiels Bohr Institute, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-9820-3567

Funding

Carlsbergfondet CF20-0046Carlsbergfondet CF23-0173Novo Nordisk Fonden NNF21CC0073729
6 · The paper itself

Abstract

SARS-CoV-2 induces delayed type-I/III interferon production, allowing it to escape the early innate immune response. The delay has been attributed to a deficiency in the ability of cells to sense viral replication upon infection, which in turn hampers activation of the antiviral state in bystander cells. Here, we introduce a cellular automaton model to investigate the spatiotemporal spreading of viral infection as a function of virus and host-dependent parameters. The model suggests that the considerable person-to-person heterogeneity in SARS-CoV-2 infections is a consequence of high sensitivity to slight variations in biological parameters near a critical threshold. It further suggests that within-host viral proliferation can be curtailed by the presence of remarkably few cells that are primed for IFN production. Thus, the observed heterogeneity in defense readiness of cells reflects a remarkably cost-efficient strategy for protection.

Indexed as

COVID-19SARS-CoV-2Epithelial CellsHumansImmunity, InnateInterferonsVirus ReplicationInterferonsanti viral statecriticalityhumanimmunologyinflammationinterferonspercolationviruses

Identifiers

PMID38941138
PMCPMC11213566

What Socratic 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 Socratic graph.