Evidence map›Paper›PMID 37009214›Full record

ArticleiScience2023

Rubella virus infection in endothelial cells reduces angiogenesis via interferon beta-induced CXCL10.

Vivien Henschke, Konstanze Hild, Erik Schilling, Jan Haas, Vanina Filipova, Stephan Erbe, Roman König, Judith M Hübschen, Ulrich Laufs, Claudia Claus and 1 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 4 institutions in 2 countries.

Vivien HenschkeInstitute of Medical Microbiology and Virology, Medical Faculty, Leipzig University, Leipzig, Germany.
Konstanze HildInstitute of Medical Microbiology and Virology, Medical Faculty, Leipzig University, Leipzig, Germany.
Erik SchillingDepartment of Internal Medicine III, Rheumatology Unit, Medical Faculty, Leipzig University, Leipzig, Germany.
Jan HaasDepartment of Internal Medicine III, University of Heidelberg, Heidelberg, Germany.
Vanina FilipovaKlinik und Poliklinik für Kardiologie, Universitätsklinikum Leipzig, 04103 Leipzig, Germany.
Stephan ErbeKlinik und Poliklinik für Kardiologie, Universitätsklinikum Leipzig, 04103 Leipzig, Germany.
Roman KönigKlinik und Poliklinik für Kardiologie, Universitätsklinikum Leipzig, 04103 Leipzig, Germany.
Judith M HübschenDepartment of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, 4354 Esch-sur-Alzette, Luxembourg.
Ulrich LaufsKlinik und Poliklinik für Kardiologie, Universitätsklinikum Leipzig, 04103 Leipzig, Germany.
Claudia ClausInstitute of Medical Microbiology and Virology, Medical Faculty, Leipzig University, Leipzig, Germany.
Jes-Niels BoeckelKlinik und Poliklinik für Kardiologie, Universitätsklinikum Leipzig, 04103 Leipzig, Germany.
University Hospital Leipzig · DELeipzig University · DEHeidelberg University · DELuxembourg Institute of Health · LU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rubella virus (RuV) infection during pregnancy can lead to abortion, stillbirth, and embryonic defects, resulting in congenital rubella syndrome (CRS). It is estimated that there are still 100,000 cases of CRS per year in developing regions with a mortality rate of over 30%. The molecular pathomechanisms remain largely unexplored. Placental endothelial cells (EC) are frequently infected with RuV. RuV reduced the angiogenic and migratory capacity of primary human EC, as confirmed by treatment of EC with serum from RuV IgM-positive patients. Next generation sequencing analysis revealed the induction of antiviral interferon (IFN) type I and III and CXCL10. The RuV-induced transcriptional profile resembled the effects of IFN-β treatment. The RuV-mediated inhibition of angiogenesis was reversed by treatment with blocking and neutralizing antibodies targeting CXCL10 and the IFN-β receptor. The data identify an important role for antiviral IFN-mediated induction of CXCL10 in the control of EC function during RuV infection.

Indexed as

ImmunologyVirology

Identifiers

PMID37009214
PMCPMC10060672
OpenAlexW4323308904

What OpenQuestion holds

Textmetadata
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.