Evidence map›Paper›PMID 12003675›Full record

ArticleJournal of cellular and molecular medicine

Molecular, immunological and clinical properties of mutated hepatitis B viruses.

C Kreutz

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Hepatology forum · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Molecular mechanisms underlying HBsAg negativity in occult HBV infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2015
    Review
  16. Article
  17. Article
  18. Atypical serological profiles in hepatitis B virus infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2013
    Review
  19. Article
  20. The underlying mechanisms for the "simultaneous HBsAg and anti-HBs serological profile".European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2011
    Review
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

1 author at 1 institution in 1 country.

C KreutzInternational Technology for Evaluation of Clinical Pharmacology, Paris, France. ckreutz@aol.com
Centre d'études et de recherches internationales de Sciences Po · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) is at the origin of severe liver diseases like chronic active hepatitis, liver cirrhosis and hepatocellular carcinoma. There are some groups of patients with high risk of generation of HBV mutants: infected infants, immunosuppressed individuals (including hemodialysis patients), patients treated with interferon and lamivudine for chronic HBV infection. These groups are the target for molecular investigations reviewed in this paper. The emergence of lamivudine- or other antiviral-resistant variants, rises concern regarding long term use of these drugs. Infection or immunization with one HBV subtype confers immunity to all subtypes. However, reinfection or reactivation of latent HBV infection with HBV mutants have been reported in patients undergoing transplant and those infected with HIV. Mutations of the viral genome which are not replicative incompetent can be selected in further course of infection or under prolonged antiviral treatment and might maintain the liver disease. Four open reading frames (ORF) which are called S-gene, C-gene, X-gene and P-gene were identified within the HBV genome. Mutations may affect each of the ORFs. Mutated S-genes were described to be responsible for HBV-infections in successfully vaccinated persons, mutated C-genes were found to provoke severe chronic liver diseases, mutated X-genes could cause serious medical problems in blood donors by escaping the conventional test systems and mutated P-genes were considered to be the reason for chemotherapeutic drug resistance. This paper reviews molecular, immunological and clinical aspects of the HBV mutants.

Indexed as

Genes, ViralMutationAnimalsEpitopes, T-LymphocyteGene Expression Regulation, ViralHepatitis BHepatitis B AntigensHepatitis B virusHumansNucleic Acid ConformationOpen Reading FramesRNA, ViralEpitopes, T-LymphocyteHepatitis B AntigensRNA, Viral

Identifiers

PMID12003675
PMCPMC6740305
OpenAlexW2026063973

What OpenQuestion holds

Textmetadata
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.