Evidence map›Paper›PMID 24701034›Full record

ArticleMediators of inflammation2014

Hantaan virus infection induces CXCL10 expression through TLR3, RIG-I, and MDA-5 pathways correlated with the disease severity.

Yusi Zhang, Bei Liu, Ying Ma, Jing Yi, Chunmei Zhang, Yun Zhang, Zhuwei Xu, Jiuping Wang, Kun Yang, Angang Yang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2014. 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
1.6field-weighted citation impact, top 18% 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, 32 citations in OpenAlex.

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  6. Frontiers in cellular and infection microbiology · 2025
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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

12 authors at 2 institutions in 1 country.

Yusi ZhangDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.ORCID 0000-0003-4272-857X
Bei LiuDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Ying MaDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Jing YiDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China ; Department of Blood Transfusion, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China.
Chunmei ZhangDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Yun ZhangDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Zhuwei XuDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Jiuping WangDepartment of Infectious Disease, Tangdu Hospital, The Fourth Military Medical University, Xi'an 710032, China.
Kun YangDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Angang YangDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Ran ZhuangDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.ORCID 0000-0002-3614-0422
Boquan JinDepartment of Immunology, The Fourth Military Medical University, 169 Changle West Road, Xi'an 710032, China.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hantaan virus (HTNV) is a major agent causing hemorrhagic fever with renal syndrome (HFRS). Although the pathogenesis of HFRS is unclear, some reports have suggested that the abundant production of proinflammatory cytokines and uncontrolled inflammatory responses may contribute to the development of HFRS. CXCL10 is one of these cytokines and is found to be involved in the pathogenesis of many virus infectious diseases. However, the role of CXCL10 in the pathogenesis of HFRS and the molecular regulation mechanism of CXCL10 in HTNV infection remain unknown. In this study, we report that CXCL10 expresses highly in the HFRS patients' sera and the elevated CXCL10 is positively correlated with the severity of HFRS. We find that HTNV, a single-strand RNA virus, can act as a double-strand RNA to activate the TLR3, RIG-I, and MDA-5 signaling pathways. Through the downstream transcription factors of these pathways, NF-κB and IRF7, which bind directly to the CXCL10's promoter, the expression of CXCL10 is increased. Our results may help to better understand the role of CXCL10 in the development of HFRS and may provide some novel insights into the immune response of HTNV infection.

Indexed as

AnimalsChemokine CXCL10Chlorocebus aethiopsDEAD Box Protein 58DEAD-box RNA HelicasesDisease ProgressionHantaan virusHemorrhagic Fever with Renal SyndromeHumansHuman Umbilical Vein Endothelial CellsInterferon-Induced Helicase, IFIH1Interferon Regulatory Factor-7LuciferasesNF-kappa BReceptors, CXCR3Receptors, ImmunologicChemokine CXCL10CXCL10 protein, humanCXCR3 protein, humanDEAD Box Protein 58DEAD-box RNA HelicasesIFIH1 protein, humanInterferon-Induced Helicase, IFIH1Interferon Regulatory Factor-7IRF7 protein, humanLuciferasesNF-kappa BReceptors, CXCR3Receptors, ImmunologicRIGI protein, humanTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID24701034
PMCPMC3950924
OpenAlexW1990288506

What OpenQuestion holds

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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.