Evidence map›Paper›PMID 30401896›Full record

ArticleEmerging microbes & infections2018

Kyasanur Forest disease virus infection activates human vascular endothelial cells and monocyte-derived dendritic cells.

Jana Sirmarova, Jiri Salat, Martin Palus, Vaclav Hönig, Helena Langhansova, Michael R Holbrook, Daniel Ruzek

Open access · goldAbstract read
In one paragraph

Article in Emerging microbes & infections, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Jana SirmarovaDepartment of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100, Brno, Czech Republic.
Jiri SalatDepartment of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100, Brno, Czech Republic.
Martin PalusDepartment of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100, Brno, Czech Republic.
Vaclav HönigDepartment of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100, Brno, Czech Republic.ORCID http://orcid.org/0000-0003-0469-4604
Helena LanghansovaInstitute of Parasitology, Biology Centre of the Czech Academy of Sciences, Branisovska 31, CZ-37005, Ceske Budejovice, Czech Republic.
Michael R HolbrookNIAID Integrated Research Facility, 8200 Research Plaza, Ft. Detrick, Frederick, MD, 21702, USA.
Daniel RuzekDepartment of Virology, Veterinary Research Institute, Hudcova 70, CZ-62100, Brno, Czech Republic. ruzekd@paru.cas.cz.ORCID http://orcid.org/0000-0003-4655-2380
Veterinary Research Institute · CZUniversity of South Bohemia in České Budějovice · CZ

Funding

Grantová Agentura České Republiky (Grant Agency of the Czech Republic) 16-20054SGrantová Agentura České Republiky (Grant Agency of the Czech Republic) 17-02196SMinisterstvo Školství, Mládeže a Tělovýchovy (Ministry of Education, Youth and Sports) CZ.02.1.01/0.0/0.0/15_003/0000495Ministerstvo Školství, Mládeže a Tělovýchovy (Ministry of Education, Youth and Sports) LO1218Ministerstvo Zdravotnictví Ceské Republiky (Ministry of Health of the Czech Republic) 16-34238A
6 · The paper itself

Abstract

Kyasanur Forest disease virus (KFDV) is a highly pathogenic tick-borne flavivirus enzootic to India. In humans, KFDV causes a severe febrile disease. In some infected individuals, hemorrhagic manifestations, such as bleeding from the nose and gums and gastrointestinal bleeding with hematemesis and/or blood in the stool, have been reported. However, the mechanisms underlying these hemorrhagic complications remain unknown, and there is no information about the specific target cells for KFDV. We investigated the interaction of KFDV with vascular endothelial cells (ECs) and monocyte-derived dendritic cells (moDCs), which are key targets for several other hemorrhagic viruses. Here, we report that ECs are permissive to KFDV infection, which leads to their activation, as demonstrated by the upregulation of E-selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 at the mRNA and protein levels. Increased expression of these adhesive molecules correlated with increased leukocyte adhesion. Infected ECs upregulated the expression of interleukin (IL)-6 but not IL-8. Additionally, moDCs were permissive to KFDV infection, leading to increased release of IL-6 and tumor necrosis factor-α. Supernatants from KFDV-infected moDCs caused EC activation, as measured by leukocyte adhesion. The results indicate that ECs and moDCs can be targets for KFDV and that both direct and indirect mechanisms can contribute to EC activation.

Indexed as

Antigens, CDCadherinsCells, CulturedDendritic CellsEncephalitis Viruses, Tick-BorneEndothelial CellsHumansIntercellular Adhesion Molecule-1Interleukin-6Interleukin-8Kyasanur Forest DiseaseRNA, MessengerTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1Antigens, CDCadherinsCDH1 protein, humanCXCL8 protein, humanICAM1 protein, humanIL6 protein, humanIntercellular Adhesion Molecule-1Interleukin-6Interleukin-8RNA, MessengerTumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID30401896
PMCPMC6220120
OpenAlexW2899393737

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.