Evidence map›Paper›PMID 28090316›Full record

ReviewClinical & translational immunology2016

The role of tumour necrosis factor in hepatitis B infection: Jekyll and Hyde.

Zina Valaydon, Marc Pellegrini, Alexander Thompson, Paul Desmond, Peter Revill, Gregor Ebert

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical & translational immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 37 citations in OpenAlex.

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  12. The immune system of the liver: 50 years of strangeness.Clinical & translational immunology · 2017
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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

6 authors at 4 institutions in 1 country.

Zina ValaydonThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia; Department of Gastroenterology, St Vincent's Hospital, Fitzroy,Victoria, Australia; Division of Research and Molecular Development, Victorian Infectious Diseases Reference Laboratory, Peter Doherty Institute, Parkville, Victoria, Australia; Department of Medicine, Eastern Hill Academic Centre, The University of Melbourne, Parkville, Victoria, Australia.
Marc PellegriniThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.
Alexander ThompsonDepartment of Gastroenterology, St Vincent's Hospital, Fitzroy,Victoria, Australia; Division of Research and Molecular Development, Victorian Infectious Diseases Reference Laboratory, Peter Doherty Institute, Parkville, Victoria, Australia; Department of Medicine, Eastern Hill Academic Centre, The University of Melbourne, Parkville, Victoria, Australia.
Paul DesmondDepartment of Gastroenterology, St Vincent's Hospital, Fitzroy,Victoria, Australia; Division of Research and Molecular Development, Victorian Infectious Diseases Reference Laboratory, Peter Doherty Institute, Parkville, Victoria, Australia; Department of Medicine, Eastern Hill Academic Centre, The University of Melbourne, Parkville, Victoria, Australia.
Peter RevillDepartment of Medicine, Eastern Hill Academic Centre, The University of Melbourne, Parkville, Victoria, Australia; Department of Microbiology and Immunology, Peter Doherty Institute, The University of Melbourne, Parkville, Victoria, Australia.
Gregor EbertThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia; Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.
Peter Doherty Institute · AUUniversity of Melbourne · AUVictorian Infectious Diseases Reference Laboratory · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic hepatitis B (CHB) is a major health problem worldwide and is associated with significant long-term morbidity and mortality. The hepatitis B virus (HBV) is a hepatotropic virus that is capable of integrating in the host nucleus permanently resulting in lifelong infection. To date, there is no definitive cure for HBV, as our current treatments cannot eradicate the viral reservoir that has integrated in the liver. Elucidating the immunopathogenesis is key to finding a therapeutic target for HBV as the virus is not in itself cytopathic but the immune response to the virus causes the majority of the cellular injury. In most cases, the virus reaches a state of equilibrium with low viral replication constrained by host immunity. Multiple cytokines have been implicated in the pathogenesis of CHB. Tumor necrosis factor (TNF) has emerged as a key player; on one hand it can facilitate immune-mediated virological control but on the other hand it can cause collateral hepatocyte damage, cirrhosis and possibly promote hepatocellular carcinoma. In this review, we discuss the current understanding of the immunopathogenesis of HBV, focusing on TNF and whether it can be harnessed in therapeutic strategies to cure HBV infection.

Identifiers

PMID28090316
PMCPMC5192060
OpenAlexW2560475594

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.