Evidence map›Paper›PMID 30166948›Full record

ArticleGastroenterology & hepatology2018

Current and Future Management of Chronic Hepatitis D.

Patrizia Farci, Grazia Anna Niro

Abstract read
In one paragraph

Article in Gastroenterology & hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Editorial: Pathogen-host interaction in the development of viral hepatitis.Frontiers in cellular and infection microbiology · 2023
    Article
  7. Article
  8. Review
  9. Review
  10. Viral hepatitis: Past, present, and future.World journal of gastroenterology · 2022
    Review
  11. Article
  12. Article
  13. Viral Hepatitis - The Road Traveled and the Journey Remaining.Hepatic medicine : evidence and research · 2022
    Review
  14. Review
  15. The evolution and clinical impact of hepatitis B virus genome diversity.Nature reviews. Gastroenterology & hepatology · 2020
    Review
  16. Review
  17. Article
  18. Article
  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.

Patrizia FarciDr Farci is chief of the Hepatic Pathogenesis Section of the Laboratory of Infectious Diseases at the National Institute of Allergy and Infectious Diseases in the National Institutes of Health in Bethesda, Maryland.
Grazia Anna NiroDr Farci is chief of the Hepatic Pathogenesis Section of the Laboratory of Infectious Diseases at the National Institute of Allergy and Infectious Diseases in the National Institutes of Health in Bethesda, Maryland.

Funding

Molecular Mechanisms of Pathogenesis of Acute and Chronic Liver DiseasesZIAAI000999 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FARCI, PATRIZIA · 2009 to 2025
$25.3M
6 · The paper itself

Abstract

Hepatitis D virus (HDV) is a defective RNA virus that requires the hepatitis B surface antigen (HBsAg) of the hepatitis B virus (HBV) for its assembly, release, and transmission. HDV is highly pathogenic, causing the least common, but most severe, form of chronic viral hepatitis at all ages. Although significant advances have been made in the treatment of chronic viral hepatitis, targeting HDV remains a major challenge because of the unconventional nature of this virus and the severity of its disease. The virus contains a ribonucleoprotein complex formed by the RNA genome with a single structural protein, delta antigen (HDAg), which exists in 2 forms (small and large HDAg) and is coated by HBsAg. Farnesylation of the large HDAg is essential for anchoring the ribonucleoprotein to HBsAg for the assembly of virion particles. HDV enters into hepatocytes by using the HBV receptor, the sodium taurocholate cotransporting polypeptide (NTCP). Unlike other RNA viruses, HDV does not encode its own polymerase but exploits the host RNA polymerase II for replication. Thus, in contrast to HBV and hepatitis C virus, which possess virus-specific enzymes that can be targeted by specific inhibitors, the lack of a virus-specific polymerase makes HDV a particularly challenging therapeutic target. Treatment of hepatitis D remains unsatisfactory, and interferon-α has been the only approved drug over the past 30 years. This article examines the unconventional nature of HDV, the current management of chronic hepatitis D, and how new insights from the HDV life cycle have led to the development of 3 novel classes of drugs (NTCP receptor inhibitors, farnesyltransferase inhibitors, and nucleic acid polymers) that are currently under clinical evaluation.

Indexed as

chronic hepatitis DHepatitis D viruslonafarnibMyrcludex Bpegylated interferonREP 2139standard interferontreatment

Identifiers

PMID30166948
PMCPMC6111511

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.