Evidence map›Paper›PMID 26134299›Full record

ArticleScientific reports2015

Host Responses and Regulation by NFκB Signaling in the Liver and Liver Epithelial Cells Infected with A Novel Tick-borne Bunyavirus.

Qiyu Sun, Cong Jin, Lili Zhu, Mifang Liang, Chuan Li, Carol J Cardona, Dexin Li, Zheng Xing

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

24 citing papers in PubMed, 31 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

8 authors at 3 institutions in 2 countries.

Qiyu SunThe State Key Laboratory of Pharmaceutical Biotechnology and Medical School, Nanjing University, Nanjing, China.
Cong JinNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Lili ZhuThe State Key Laboratory of Pharmaceutical Biotechnology and Medical School, Nanjing University, Nanjing, China.
Mifang LiangNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Chuan LiNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Carol J CardonaVeterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Twin Cities, Saint Paul, MN, USA.
Dexin LiNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Zheng Xing1] The State Key Laboratory of Pharmaceutical Biotechnology and Medical School, Nanjing University, Nanjing, China [2] Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Twin Cities, Saint Paul, MN, USA.
National Institute for Viral Disease Control and Prevention · CNChina Pharmaceutical University · CNUniversity of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection in humans by severe fever with thrombocytopenia syndrome virus (SFTSV), a novel bunyavirus transmitted by ticks, is often associated with pronounced liver damage, especially in fatal cases. Little has been known, however, about how liver cells respond to SFTSV and how the response is regulated. In this study we report that proinflammatory cytokines were induced in liver tissues of C57/BL6 mice infected with SFTSV, which may cause tissue necrosis in mice. Human liver epithelial cells were susceptible to SFTSV and antiviral interferon (IFN) and IFN-inducible proteins were induced upon infection. We observed that infection of liver epithelial cells led to significant increases in proinflammatory cytokines and chemokines, including IL-6, RANTES, IP-10, and MIP-3a, which were regulated by NFκB signaling, and the activation of NFκB signaling during infection promoted viral replication in liver epithelial cells. Viral nonstructural protein NSs was inhibitory to the induction of IFN-β, but interestingly, NFκB activation was enhanced in the presence of NSs. Therefore, NSs plays dual roles in the suppression of antiviral IFN-β induction as well as the promotion of proinflammatory responses. Our findings provide the first evidence for elucidating host responses and regulation in liver epithelial cells infected by an emerging bunyavirus.

Indexed as

AnimalsBunyaviridae InfectionsChemokine CCL20Chemokine CCL5Chemokine CXCL10Epithelial CellsGene Expression RegulationHost-Pathogen InteractionsHumansInterleukin-6LiverMiceNF-kappa BOrthobunyavirusTick-Borne DiseasesCcl5 protein, mouseChemokine CCL20Chemokine CCL5Chemokine CXCL10Cxcl10 protein, mouseInterleukin-6NF-kappa B

Identifiers

PMID26134299
PMCPMC4488873
OpenAlexW2256319867

What OpenQuestion holds

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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.