Evidence map›Paper›PMID 15163707›Full record

ArticleJournal of virology2004

Differential antiviral response of endothelial cells after infection with pathogenic and nonpathogenic hantaviruses.

Annette A Kraus, Martin J Raftery, Thomas Giese, Rainer Ulrich, Rainer Zawatzky, Stefan Hippenstiel, Norbert Suttorp, Detlev H Krüger, Günther Schönrich

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 106 citations in OpenAlex.

  1. Roles of endothelial cells during infection.Current opinion in immunology · 2025
    Review
  2. Article
  3. Article
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  7. Review
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  9. Review
  10. Article
  11. Article
  12. Article
  13. Endothelial Cells in Emerging Viral Infections.Frontiers in cardiovascular medicine · 2021
    Review
  14. Article
  15. Orthohantavirus Pathogenesis and Cell Tropism.Frontiers in cellular and infection microbiology · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 4 institutions in 2 countries.

Annette A KrausInstitut für Virologie, Charité-Universitätsmedizin Berlin, Schumannstrasse 20/21, D-10098 Berlin, Germany.
Martin J Raftery
Thomas Giese
Rainer Ulrich
Rainer Zawatzky
Stefan Hippenstiel
Norbert Suttorp
Detlev H Krüger
Günther Schönrich
Institut de Virologie · FRCharité - Universitätsmedizin Berlin · DEDKFZ-ZMBH Alliance · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hantaviruses represent important human pathogens and can induce hemorrhagic fever with renal syndrome (HFRS), which is characterized by endothelial dysfunction. Both pathogenic and nonpathogenic hantaviruses replicate without causing any apparent cytopathic effect, suggesting that immunopathological mechanisms play an important role in pathogenesis. We compared the antiviral responses triggered by Hantaan virus (HTNV), a pathogenic hantavirus associated with HFRS, and Tula virus (TULV), a rather nonpathogenic hantavirus, in human umbilical vein endothelial cells (HUVECs). Both HTNV- and TULV-infected cells showed increased levels of molecules involved in antigen presentation. However, TULV-infected HUVECs upregulated HLA class I molecules more rapidly. Interestingly, HTNV clearly induced the production of beta interferon (IFN-beta), whereas expression of this cytokine was barely detectable in the supernatant or in extracts from TULV-infected HUVECs. Nevertheless, the upregulation of HLA class I on both TULV- and HTNV-infected cells could be blocked by neutralizing anti-IFN-beta antibodies. Most strikingly, the antiviral MxA protein, which interferes with hantavirus replication, was already induced 16 h after infection with TULV. In contrast, HTNV-infected HUVECs showed no expression of MxA until 48 h postinfection. In accordance with the kinetics of MxA expression, TULV replicated only inefficiently in HUVECs, whereas HTNV-infected cells produced high titers of virus particles that decreased after 48 h postinfection. Both hantavirus species, however, could replicate equally well in Vero E6 cells, which lack an IFN-induced MxA response. Thus, delayed induction of antiviral MxA in endothelial cells after infection with HTNV could allow viral dissemination and contribute to the pathogenesis leading to HFRS.

Indexed as

AnimalsChlorocebus aethiopsEndothelial CellsGTP-Binding ProteinsHantaan virusHistocompatibility Antigens Class IHumansInterferon-betaMyxovirus Resistance ProteinsOrthohantavirusUmbilical VeinsVero CellsVirus ReplicationGTP-Binding ProteinsHistocompatibility Antigens Class IInterferon-betaMX1 protein, humanMyxovirus Resistance Proteins

Identifiers

PMID15163707
PMCPMC416501
OpenAlexW2132053307

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.