Evidence map›Paper›PMID 42234680›Full record

ArticlePloS one2026

MAVS is important for antiviral defense against influenza A virus in a human respiratory epithelium model.

Maja Hemberg, Anne Louise Hansen, Jacob Storgaard, Julia Blay-Cadanet, Alice Pedersen, Anne Laugaard Thielke, Christian Kanstrup Holm

Abstract read
In one paragraph

Article in PloS one, 2026. 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
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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

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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

7 authors.

Maja HembergDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID https://orcid.org/0009-0002-9476-5284
Anne Louise HansenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Jacob StorgaardDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Julia Blay-CadanetDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Alice PedersenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Anne Laugaard ThielkeDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Christian Kanstrup HolmDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID https://orcid.org/0000-0002-2655-3362

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The respiratory epithelium is an important immunological barrier and the first line of defense against influenza A virus (IAV). In mice and in various cellular systems, induction of type I interferons (IFNα/β) during IAV infections is known to depend on cytosolic RNA sensors retinoic acid-induced gene I (RIG-I) and melanoma differentiation-association gene 5 (MDA5) and their common adaptor protein mitochondrial antiviral-signaling adaptor protein (MAVS). Until now, it has not been possible to directly assess the importance of MAVS for induction of IFNs and for resistance to IAV infection in primary human respiratory epithelium. Here, we used CRISPR-Cas9 to establish MAVS-deficient cultures of primary human respiratory epithelium using the air-liquid interphase culture system. Using this setup, we show that MAVS is indeed required for the induction of type I and type III IFNs and subsequently for the induction of IFN-stimulated genes in response to IAV infection in this respiratory epithelium model. Finally, we demonstrate that MAVS is important for restricting viral replication in this model. In conclusion, this study demonstrates that MAVS plays a non-redundant protective role during IAV infection in primary human respiratory epithelium.

Indexed as

Adaptor Proteins, Signal TransducingInfluenza A virusInfluenza, HumanRespiratory MucosaAnimalsCells, CulturedCRISPR-Cas SystemsHumansInterferonsInterferon Type IVirus ReplicationAdaptor Proteins, Signal TransducingInterferonsInterferon Type IMAVS protein, human

Identifiers

PMID42234680
PMCPMC13232818

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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.