Evidence map›Paper›PMID 28886065›Full record

ArticlePloS one2017

Hepatitis C virus mediated chronic inflammation and tumorigenesis in the humanised immune system and liver mouse model.

Zhiqiang Zheng, Ching Wooen Sze, Choong Tat Keng, Muthafar Al-Haddawi, Min Liu, Sue Yee Tan, Hwee Ling Kwek, Zhisheng Her, Xue Ying Chan, Bhaskar Barnwal and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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  7. Host immune response in chronic hepatitis C infection: involvement of cytokines and inflammasomes.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie · 2020
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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

15 authors at 3 institutions in 2 countries.

Zhiqiang ZhengInstitute of Molecular and Cell Biology, Singapore, Singapore.ORCID http://orcid.org/0000-0003-1028-3246
Ching Wooen SzeDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University Health System, National University of Singapore, Singapore, Singapore.
Choong Tat KengInstitute of Molecular and Cell Biology, Singapore, Singapore.
Muthafar Al-HaddawiInstitute of Molecular and Cell Biology, Singapore, Singapore.
Min LiuInstitute of Molecular and Cell Biology, Singapore, Singapore.
Sue Yee TanInstitute of Molecular and Cell Biology, Singapore, Singapore.
Hwee Ling KwekInstitute of Molecular and Cell Biology, Singapore, Singapore.
Zhisheng HerInstitute of Molecular and Cell Biology, Singapore, Singapore.
Xue Ying ChanInstitute of Molecular and Cell Biology, Singapore, Singapore.
Bhaskar BarnwalInstitute of Molecular and Cell Biology, Singapore, Singapore.
Eva LohDepartment of Pathology and Laboratory Medicine, KK Women's and Children's Hospital, Singapore, Singapore.
Kenneth Tou En ChangDepartment of Pathology and Laboratory Medicine, KK Women's and Children's Hospital, Singapore, Singapore.
Thiam Chye TanDuke-NUS Graduate Medical School, Singapore, Singapore.
Yee-Joo TanInstitute of Molecular and Cell Biology, Singapore, Singapore.
Qingfeng ChenInstitute of Molecular and Cell Biology, Singapore, Singapore.
Institute of Molecular and Cell Biology · SGKK Women's and Children's Hospital · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C is a liver disease caused by infection of the Hepatitis C virus (HCV). Many individuals infected by the virus are unable to resolve the viral infection and develop chronic hepatitis, which can lead to formation of liver cirrhosis and cancer. To understand better how initial HCV infections progress to chronic liver diseases, we characterised the long term pathogenic effects of HCV infections with the use of a humanised mouse model (HIL mice) we have previously established. Although HCV RNA could be detected in infected mice up to 9 weeks post infection, HCV infected mice developed increased incidences of liver fibrosis, granulomatous inflammation and tumour formation in the form of hepatocellular adenomas or hepatocellular carcinomas by 28 weeks post infection compared to uninfected mice. We also demonstrated that chronic liver inflammation in HCV infected mice was mediated by the human immune system, particularly by monocytes/macrophages and T cells which exhibited exhaustion phenotypes. In conclusion, HIL mice can recapitulate some of the clinical symptoms such as chronic inflammation, immune cell exhaustion and tumorigenesis seen in HCV patients. Our findings also suggest that persistence of HCV-associated liver disease appear to require initial infections of HCV and immune responses but not long term HCV viraemia.

Indexed as

Cell Transformation, NeoplasticHepacivirusAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticBiomarkersCarcinoma, HepatocellularCD68 MoleculeCytokinesDisease Models, AnimalHepatitis C, ChronicLiver Function TestsLiver NeoplasmsMacrophagesMiceMonocytesAntigens, CDAntigens, Differentiation, MyelomonocyticBiomarkersCD68 antigen, humanCD68 MoleculeCytokinesSerum Albumin

Identifiers

PMID28886065
PMCPMC5590885
OpenAlexW2752193047

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.