Evidence map›Paper›PMID 33974679›Full record

ArticlePLoS pathogens2021

Infection of humanized mice with a novel phlebovirus presented pathogenic features of severe fever with thrombocytopenia syndrome.

Shijie Xu, Na Jiang, Waqas Nawaz, Bingxin Liu, Fang Zhang, Ye Liu, Xilin Wu, Zhiwei Wu

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  6. Investigation into the Pancreatic Pathogenesis of SFTSV across Multiple Levels.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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 2 institutions in 1 country.

Shijie XuCenter for Public Health Research, Medical School, Nanjing University, Nanjing, China.
Na JiangCenter for Public Health Research, Medical School, Nanjing University, Nanjing, China.
Waqas NawazCenter for Public Health Research, Medical School, Nanjing University, Nanjing, China.
Bingxin LiuCenter for Public Health Research, Medical School, Nanjing University, Nanjing, China.
Fang ZhangCenter for Public Health Research, Medical School, Nanjing University, Nanjing, China.
Ye LiuCenter for Public Health Research, Medical School, Nanjing University, Nanjing, China.
Xilin WuCenter for Public Health Research, Medical School, Nanjing University, Nanjing, China.ORCID 0000-0002-2829-6654
Zhiwei WuSchool of Life Sciences, Ningxia University, Yinchuan, P.R. China.
Nanjing Medical University · CNNingxia University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe fever with thrombocytopenia syndrome virus (SFTSV) is a tick-borne emerging phlebovirus with high mortality rates of 6.0 to 30%. SFTSV infection is characterized by high fever, thrombocytopenia, leukopenia, hemorrhage and multiple organ failures. Currently, specific therapies and vaccines remain elusive. Suitable small animal models are urgently needed to elucidate the pathogenesis and evaluate the potential drug and vaccine for SFTSV infection. Previous models presented only mild or no pathogenesis of SFTS, limiting their applications in SFTSV infection. Therefore, it is an urgent need to develop a small animal model for the investigation of SFTSV pathogenesis and evaluation of therapeutics. In the current report, we developed a SFTSV infection model based on the HuPBL-NCG mice that recapitulates many pathological characteristics of SFTSV infection in humans. Virus-induced histopathological changes were identified in spleen, lung, kidney, and liver. SFTSV was colocalized with macrophages in the spleen and liver, suggesting that the macrophages in the spleen and liver could be the principle target cells of SFTSV. In addition, histological analysis showed that the vascular endothelium integrity was severely disrupted upon viral infection along with depletion of platelets. In vitro cellular assays further revealed that SFTSV infection increased the vascular permeability of endothelial cells by promoting tyrosine phosphorylation and internalization of the adhesion molecule vascular endothelial (VE)-cadherin, a critical component of endothelial integrity. In addition, we found that both virus infection and pathogen-induced exuberant cytokine release dramatically contributed to the vascular endothelial injury. We elucidated the pathogenic mechanisms of hemorrhage syndrome and developed a humanized mouse model for SFTSV infection, which should be helpful for anti-SFTSV therapy and pathogenesis study.

Indexed as

Disease Models, AnimalAnimalsBlood PlateletsCell Adhesion MoleculesEndothelial CellsFemaleHumansLeukocytes, MononuclearMacrophagesMicePhlebovirusPhosphorylationSevere Fever with Thrombocytopenia SyndromeTick-Borne DiseasesCell Adhesion Molecules

Identifiers

PMID33974679
PMCPMC8139491
OpenAlexW3160302091

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.