Evidence map›Paper›PMID 32380149›Full record

ReviewAntiviral research2020

HBV replication inhibitors.

Claire Pierra Rouviere, Cyril B Dousson, John E Tavis

Abstract readReview
In one paragraph

Review in Antiviral research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Discovery ofInternational journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Efficacy andAntimicrobial agents and chemotherapy · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Molecules (Basel, Switzerland) · 2024
    Article
  16. Article
  17. Review
  18. Review
  19. The progress of molecules and strategies for the treatment of HBV infection.Frontiers in cellular and infection microbiology · 2023
    Review
  20. 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

3 authors.

Claire Pierra RouviereAi-biopharma, Medicinal Chemistry Department, Montpellier, France.
Cyril B DoussonAi-biopharma, Medicinal Chemistry Department, Montpellier, France. Electronic address: cyril.dousson@ai-biopharma.com.
John E TavisDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Saint Louis, MO, USA. Electronic address: John.tavis@health.slu.edu.

Funding

Optimization of alpha-hydroxytropolones as novel inhibitors of the HBV RNaseHR01AI122669 · NIAID · SAINT LOUIS UNIVERSITY · PI TAVIS, JOHN E · 2016 to 2020
$2.2M
Defining approaches for improving HID and HPD compounds as HBV RNaseH antagonistsR21AI124672 · NIAID · SAINT LOUIS UNIVERSITY · PI MEYERS, MARVIN J, TAVIS, JOHN E · 2017 to 2018
$417k
NIAID NIH HHS R01 AI122669NIAID NIH HHS R21 AI124672
6 · The paper itself

Abstract

Chronic Hepatitis B Virus infections afflict >250 million people and kill nearly 1 million annually. Current non-curative therapies are dominated by nucleos(t)ide analogs (NAs) that profoundly but incompletely suppress DNA synthesis by the viral reverse transcriptase. Residual HBV replication during NA therapy contributes to maintenance of the critical nuclear reservoir of the HBV genome, the covalently-closed circular DNA, and to ongoing infection of naive cells. Identification of next-generation NAs with improved efficacy and safety profiles, often through novel prodrug approaches, is the primary thrust of ongoing efforts to improve HBV replication inhibitors. Inhibitors of the HBV ribonuclease H, the other viral enzymatic activity essential for viral genomic replication, are in preclinical development. The complexity of HBV's reverse transcription pathway offers many other potential targets. HBV's protein-priming of reverse transcription has been briefly explored as a potential target, as have the host chaperones necessary for function of the HBV reverse transcriptase. Improved inhibitors of HBV reverse transcription would reduce HBV's replication-dependent persistence mechanisms and are therefore expected to become a backbone of future curative combination anti-HBV therapies.

Indexed as

AnimalsAntiviral AgentsClinical Trials as TopicHepatitis B, ChronicHepatitis B virusHumansMiceNucleic Acid Synthesis InhibitorsNucleosidesRibonuclease HVirus ReplicationAntiviral AgentsNucleic Acid Synthesis InhibitorsNucleosidesRibonuclease HChronic hepatitis BHepatitis B virusNucleos(t)ide analogsReverse transcriptase inhibitorsRibonuclease H inhibitors

Identifiers

PMID32380149
PMCPMC7293572

What OpenQuestion holds

Textmetadata
LicenceTDM
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.