Evidence map›Paper›PMID 35262371›Full record

ArticleJournal of virology2022

Increased Sensitivity of SARS-CoV-2 to Type III Interferon in Human Intestinal Epithelial Cells.

Camila Metz-Zumaran, Carmon Kee, Patricio Doldan, Cuncai Guo, Megan L Stanifer, Steeve Boulant

Abstract read
In one paragraph

Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Review
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  3. Mechanisms of Differential Signal Transduction by IFNLR1 Variants.bioRxiv : the preprint server for biology · 2025
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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

6 authors.

Camila Metz-Zumaran *Department of Infectious Diseases, Virology, Heidelberg University, Heidelberg, Germany.
Carmon Kee *Department of Infectious Diseases, Virology, Heidelberg University, Heidelberg, Germany.ORCID 0000-0001-5847-5509
Patricio Doldan *Department of Infectious Diseases, Virology, Heidelberg University, Heidelberg, Germany.
Cuncai GuoDepartment of Infectious Diseases, Virology, Heidelberg University, Heidelberg, Germany.
Megan L StaniferDepartment of Infectious Diseases, Molecular Virology, Heidelberg University, Heidelberg, Germany.
Steeve BoulantDepartment of Infectious Diseases, Virology, Heidelberg University, Heidelberg, Germany.ORCID 0000-0001-8614-4993

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The coronavirus SARS-CoV-2 caused the COVID-19 global pandemic leading to 5.3 million deaths worldwide as of December 2021. The human intestine was found to be a major viral target which could have a strong impact on virus spread and pathogenesis since it is one of the largest organs. While type I interferons (IFNs) are key cytokines acting against systemic virus spread, in the human intestine type III IFNs play a major role by restricting virus infection and dissemination without disturbing homeostasis. Recent studies showed that both type I and III IFNs can inhibit SARS-CoV-2 infection, but it is not clear whether one IFN controls SARS-CoV-2 infection of the human intestine better or with a faster kinetics. In this study, we could show that type I and III IFNs both possess antiviral activity against SARS-CoV-2 in human intestinal epithelial cells (hIECs); however, type III IFN is more potent. Shorter type III IFN pretreatment times and lower concentrations were required to efficiently reduce virus load compared to type I IFNs. Moreover, type III IFNs significantly inhibited SARS-CoV-2 even 4 h postinfection and induced a long-lasting antiviral effect in hIECs. Importantly, the sensitivity of SARS-CoV-2 to type III IFNs was virus specific since type III IFN did not control VSV infection as efficiently. Together, these results suggest that type III IFNs have a higher potential for IFN-based treatment of SARS-CoV-2 intestinal infection compared to type I IFNs.

Indexed as

COVID-19 Drug TreatmentInterferonsInterferon Type ISARS-CoV-2Antiviral AgentsCells, CulturedEpithelial CellsHumansInterferon LambdaAntiviral AgentsInterferon LambdaInterferonsInterferon Type Ihuman intestinal epithelial cellsinterferoninterferon lambdaintrinsic immune responseSARS-CoV-2type III interferon

Identifiers

PMID35262371
PMCPMC9006957

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.