Evidence map›Paper›PMID 24409335›Full record

ReviewWorld journal of hepatology2013

Life cycle and pathogenesis of hepatitis D virus: A review.

Zaigham Abbas, Rafia Afzal

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of hepatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Virus Behavior after UVMicroorganisms · 2023
    Article
  10. Hepatitis Delta Infection: A Clinical Review.Seminars in liver disease · 2023
    Review
  11. Diagnosis of HDV: From virology to non-invasive markers of fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Viral hepatitis: Past, present, and future.World journal of gastroenterology · 2022
    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 1 institution in 1 country.

Zaigham AbbasZaigham Abbas, Rafia Afzal, Department of Hepatogastroenterology, Sindh Institute of Urology and Transplantation, Karachi 75500, Pakistan.
Rafia AfzalZaigham Abbas, Rafia Afzal, Department of Hepatogastroenterology, Sindh Institute of Urology and Transplantation, Karachi 75500, Pakistan.
Sindh Institute of Urology and Transplantation · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis D virus (HDV) is a defective RNA virus which requires the help of hepatitis B virus (HBV) virus for its replication and assembly of new virions. HDV genome contains only one actively transcribed open reading frame which encodes for two isoforms of hepatitis delta antigen. Post-translational modifications of small and large delta antigens (S-HDAg and L-HDAg) involving phosphorylation and isoprenylation respectively confer these antigens their specific properties. S-HDAg is required for the initiation of the viral genome replication, whereas L-HDAg serves as a principal inhibitor of replication and is essential for the assembly of new virion particles. Immune mediation has usually been implicated in HDV-associated liver damage. The pathogenesis of HDV mainly involves interferon-α signaling inhibition, HDV-specific T-lymphocyte activation and cytokine responses, and tumor necrosis factor-alpha and nuclear factor kappa B signaling. Due to limited protein coding capacity, HDV makes use of host cellular proteins to accomplish their life cycle processes, including transcription, replication, post-transcriptional and translational modifications. This intimate host-pathogen interaction significantly alters cell proteome and is associated with an augmented expression of pro-inflammatory, growth and anti-apoptotic factors which explains severe necroinflammation and increased cell survival and an early progression to hepatocellular carcinoma in HDV patients. The understanding of the process of viral replication, HBV-HDV interactions, and etio-pathogenesis of the severe course of HDV infection is helpful in identifying the potential therapeutic targets in the virus life cycle for the prophylaxis and treatment of HDV infection and complications.

Indexed as

Hepatitis B virusHepatitis delta antigensHepatitis D virusHepatitis D virus pathogenicityHepatocellular carcinomaHost-pathogen interactionsInterferon-alphaVirus replication

Identifiers

PMID24409335
PMCPMC3879688
OpenAlexW2013867248

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.