Evidence map›Paper›PMID 37112941›Full record

ArticleViruses2023

Analysis of Nipah Virus Replication and Host Proteome Response Patterns in Differentiated Porcine Airway Epithelial Cells Cultured at the Air-Liquid Interface.

Martin Müller, Kerstin Fischer, Elisabeth Woehnke, Luca M Zaeck, Christoph Prönnecke, Michael R Knittler, Axel Karger, Sandra Diederich, Stefan Finke

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
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.

Martin MüllerInstitute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany.
Kerstin FischerInstitute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany.ORCID 0000-0002-8707-3442
Elisabeth WoehnkeInstitute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany.
Luca M ZaeckInstitute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany.ORCID 0000-0001-7997-493X
Christoph PrönneckeCentre for Biotechnology and Biomedicine, Molecular Biological-Biochemical Processing Technology, Leipzig University, 04103 Leipzig, Germany.
Michael R KnittlerInstitute of Immunology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Greifswald-Insel Riems, Germany.ORCID 0000-0002-1603-9861
Axel KargerInstitute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany.ORCID 0000-0002-0054-7394
Sandra DiederichInstitute of Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany.ORCID 0000-0001-6740-3312
Stefan FinkeInstitute of Molecular Virology and Cell Biology, Friedrich-Loeffler-Institut, Federal Research Institute of Animal Health, 17493 Greifswald-Insel Riems, Germany.ORCID 0000-0001-8716-2341
Friedrich-Loeffler-Institut · DELeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory tract epithelium infection plays a primary role in Nipah virus (NiV) pathogenesis and transmission. Knowledge about infection dynamics and host responses to NiV infection in respiratory tract epithelia is scarce. Studies in non-differentiated primary respiratory tract cells or cell lines indicate insufficient interferon (IFN) responses. However, studies are lacking in the determination of complex host response patterns in differentiated respiratory tract epithelia for the understanding of NiV replication and spread in swine. Here we characterized infection and spread of NiV in differentiated primary porcine bronchial epithelial cells (PBEC) cultivated at the air-liquid interface (ALI). After the initial infection of only a few apical cells, lateral spread for 12 days with epithelium disruption was observed without releasing substantial amounts of infectious virus from the apical or basal sides. Deep time course proteomics revealed pronounced upregulation of genes related to type I/II IFN, immunoproteasomal subunits, transporter associated with antigen processing (TAP)-mediated peptide transport, and major histocompatibility complex (MHC) I antigen presentation. Spliceosomal factors were downregulated. We propose a model in which NiV replication in PBEC is slowed by a potent and broad type I/II IFN host response with conversion from 26S proteasomes to immunoproteasomal antigen processing and improved MHC I presentation for adaptive immunity priming. NiV induced cytopathic effects could reflect the focal release of cell-associated NiV, which may contribute to efficient airborne viral spread between pigs.

Indexed as

Nipah VirusAnimalsCells, CulturedEpithelial CellsProteomeRespiratory MucosaSwineVirus ReplicationProteomeair–liquid interface cultureimmune responsemass spectrometryNipah virusrespiratory epithelium

Identifiers

PMID37112941
PMCPMC10143807
OpenAlexW4365514905

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.