Evidence map›Paper›PMID 27190317›Full record

ReviewClinical infectious diseases : an official publication of the Infectious Diseases Society of America2016

Mechanism of Hepatitis B Virus Persistence in Hepatocytes and Its Carcinogenic Potential.

Maura Dandri, Joerg Petersen

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04724785 (Real World Study on the Effect of HBV-DNA High-precision Detection Based Anti-viral Regimen Adjustment on Achieving Complete Virologic Response in Patients With Chronic Hepatitis B.), which is not on this map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-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.

NCT04724785 unknown statusnot on this mapstarted 2020, after this paper: background citation

Real World Study on the Effect of HBV-DNA High-precision Detection Based Anti-viral Regimen Adjustment on Achieving Complete Virologic Response in Patients With Chronic Hepatitis B.(REACH)

TypeobservationalSponsorThe Second Affiliated Hospital of Chongqing Medical UniversityRan2020 to 2022Enrolled10,000ConditionsSustained Virologic Response, Hepatitis B, ChronicArmsonly monitoring, monitoring and regimen change if necessary, regimen change
3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Hepatitis B virus-induced hepatocellular carcinoma: a persistent global problem.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
    Review
  11. Review
  12. Frequency of Hepatitis B Markers in Systemic Lupus Erythematosus Patients in Iran.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. 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

2 authors at 2 institutions in 1 country.

Maura DandriI Department of Internal Medicine, University Medical Center Hamburg-Eppendorf German Center for Infection Research, Hamburg-Lübeck-Borstel site.
Joerg PetersenIFI Institute for Interdisciplinary Medicine, Asklepios Clinic St Georg, Hamburg, Germany.
Asklepios · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver disease associated with persistent infection with hepatitis B virus (HBV) continues to be a major health problem of global impact. Despite the existence of an effective vaccine, at least 240 million people are chronically infected worldwide, and are at risk of developing liver cirrhosis and hepatocellular carcinoma. Although chronic HBV infection is considered the main risk factor for liver cancer development, the molecular mechanisms determining persistence of infection and long-term pathogenesis are not fully elucidated but appear to be multifactorial. Current therapeutic regimens based on the use of polymerase inhibitors can efficiently suppress viral replication but are unable to eradicate the infection. This is due both to the persistence of the HBV genome, which forms a stable minichromosome, the covalently closed circular DNA (cccDNA), in the nucleus of infected hepatocytes, as well as to the inability of the immune system to efficiently counteract chronic HBV infection. In this regard, the unique replication strategies adopted by HBV and viral protein production also appear to contribute to infection persistence by limiting the effectiveness of innate responses. The availability of improved experimental systems and molecular techniques have started to provide new information about the complex network of interactions that HBV establishes within the hepatocyte and that may contribute to disease progression and tumor development. Thus, this review will mostly focus on events involving the hepatocyte: the only target cell where HBV infection and replication take place.

Indexed as

Hepatitis BHepatitis B virusLiver NeoplasmsDNA, CircularDNA, ViralGenome, ViralHepatocytesHost-Pathogen InteractionsHumansDNA, CircularDNA, ViralDNAhepatitis Bmolecular techniques

Identifiers

PMID27190317
PMCPMC4889895
OpenAlexW2399483311

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.