Evidence map›Paper›PMID 28646094›Full record

ArticleGut2018

Immune-mediated effects targeting hepatitis C virus in a syngeneic replicon cell transplantation mouse model.

Sepideh Levander, Fredrik Holmström, Lars Frelin, Gustaf Ahlén, Daniel Rupp, Gang Long, Ralf Bartenschlager, Matti Sällberg

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. PLK1-ELAVL1/HuR-miR-122 signaling facilitates hepatitis C virus proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  2. Article
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 5 institutions in 3 countries.

Sepideh LevanderDepartment of Laboratory Medicine, Division of Clinical Microbiology, F68, Karolinska Institutet, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Solna, Sweden.
Fredrik HolmströmDepartment of Laboratory Medicine, Division of Clinical Microbiology, F68, Karolinska Institutet, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Solna, Sweden.
Lars FrelinDepartment of Laboratory Medicine, Division of Clinical Microbiology, F68, Karolinska Institutet, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Solna, Sweden.
Gustaf AhlénDepartment of Laboratory Medicine, Division of Clinical Microbiology, F68, Karolinska Institutet, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Solna, Sweden.
Daniel RuppDepartment of Infectious Diseases, Molecular Virology, University of Heidelberg, Heidelberg, Germany.
Gang LongDepartment of Infectious Diseases, Molecular Virology, University of Heidelberg, Heidelberg, Germany.
Ralf Bartenschlager *Department of Infectious Diseases, Molecular Virology, University of Heidelberg, Heidelberg, Germany.
Matti Sällberg *Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEGerman Center for Infection Research · DEHeidelberg University · DEInstitut Pasteur of Shanghai · CNKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveHCV is characterised by its ability to establish chronic infection in hepatocytes and to replicate in the presence of an inflammation. We mimicked this situation in vivo in immune-competent mice by syngeneic transplantation of HCV replicon-containing mouse hepatoma cells.

designA total of 5 million H-2

resultsHCV replicon and NS3/4A hepatoma cells generated solid tumours in vivo. Similar to what is seen in human HCV infection did HCV RNA replicate in the presence of inflammation. NS3/4A-specific CD8+ T cells seemed to transiently reduce HCV RNA levels. Both CD4+ and CD8+ T cells were required for protection against tumour growth. Vaccine-induced NS3/4A(gt2a)-specific T cells protected against HCV replicon tumours in wild-type, but not in HCV NS3/4A(gt1a)-transgenic mice with dysfunctional HCV-specific T cells. Importantly, as in human HCV infection, HCV replicon cells neither primed nor boosted a strong NS3/4A-specific T cell response.

conclusionSyngeneic transplantation of mouse HCV replicon cells into immune-competent animals mirrors many in vivo events in humans. This system is versatile and can be applied to any genetically modified H-2

Indexed as

Cell TransplantationDisease Models, AnimalHepacivirusAnimalsCarcinoma, HepatocellularHepatitis CHepatocytesMiceRepliconSerine ProteasesViral Nonstructural ProteinsNS3-4A serine protease, Hepatitis C virusSerine ProteasesViral Nonstructural ProteinsHCV repliconimmune competentmouse modelT cellsvaccine

Identifiers

PMID28646094
PMCPMC6204962
OpenAlexW2697811374

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.