Evidence map›Paper›PMID 26426038›Full record

ReviewViruses2015

Inhibitors of the Hepatitis C Virus Polymerase; Mode of Action and Resistance.

Auda A Eltahla, Fabio Luciani, Peter A White, Andrew R Lloyd, Rowena A Bull

Abstract readReview
In one paragraph

Review in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing 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

63 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. [Diagnostic value of novel hepatic fibrosis markers in assessing cirrhosis in patients with chronic hepatitis C].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. RdRp inhibitors and COVID-19: Is molnupiravir a good option?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Article

3 more citing papers are in PubMed but not listed here.

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

5 authors.

Auda A EltahlaSystems Medicine, Inflammation and Infection Research Centre, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia. a.eltahla@unsw.edu.au.
Fabio LucianiSystems Medicine, Inflammation and Infection Research Centre, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia. luciani@unsw.edu.au.
Peter A WhiteSchool of Biotechnology and Biomolecular Sciences, Faculty of Science, University of New South Wales, Sydney 2052, Australia. p.white@unsw.edu.au.
Andrew R LloydSystems Medicine, Inflammation and Infection Research Centre, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia. a.lloyd@unsw.edu.au.
Rowena A BullSystems Medicine, Inflammation and Infection Research Centre, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia. r.bull@unsw.edu.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hepatitis C virus (HCV) is a pandemic human pathogen posing a substantial health and economic burden in both developing and developed countries. Controlling the spread of HCV through behavioural prevention strategies has met with limited success and vaccine development remains slow. The development of antiviral therapeutic agents has also been challenging, primarily due to the lack of efficient cell culture and animal models for all HCV genotypes, as well as the large genetic diversity between HCV strains. On the other hand, the use of interferon-α-based treatments in combination with the guanosine analogue, ribavirin, achieved limited success, and widespread use of these therapies has been hampered by prevalent side effects. For more than a decade, the HCV RNA-dependent RNA polymerase (RdRp) has been targeted for antiviral development, and direct-acting antivirals (DAA) have been identified which bind to one of at least six RdRp inhibitor-binding sites, and are now becoming a mainstay of highly effective and well tolerated antiviral treatment for HCV infection. Here we review the different classes of RdRp inhibitors and their mode of action against HCV. Furthermore, the mechanism of antiviral resistance to each class is described, including naturally occurring resistance-associated variants (RAVs) in different viral strains and genotypes. Finally, we review the impact of these RAVs on treatment outcomes with the newly developed regimens.

Indexed as

Drug Resistance, ViralMutationAntiviral AgentsHepacivirusHepatitis C, ChronicHumansRNA-Dependent RNA PolymeraseTreatment OutcomeViral Nonstructural ProteinsAntiviral AgentsNS-5 protein, hepatitis C virusRNA-Dependent RNA PolymeraseViral Nonstructural Proteinsantiviral resistancedirect-acting antiviralhepatitis C virusNS5Bpolymerase inhibitorRNA dependent RNA polymerase

Identifiers

PMID26426038
PMCPMC4632376

What OpenQuestion holds

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LicenceCC BY
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.