Evidence map›Paper›PMID 24091203›Full record

ReviewAntiviral research2013

Host-targeting agents in the treatment of hepatitis C: a beginning and an end?

James M Baugh, Jose A Garcia-Rivera, Philippe A Gallay

Open access · greenAbstract readReview
In one paragraph

Review in Antiviral research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Entry Inhibitors of Hepatitis C Virus.Advances in experimental medicine and biology · 2022
    Article
  5. Cyclophilin A: a key player for etiological agent infection.Applied microbiology and biotechnology · 2021
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Hepatitis C virus: life cycle in cells, infection and host response, and analysis of molecular markers influencing the outcome of infection and response to therapy.Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2016
    Review
  15. Review
  16. Entry inhibitors: New advances in HCV treatment.Emerging microbes & infections · 2016
    Review
  17. Article
  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

3 authors at 1 institution in 1 country.

James M BaughDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Jose A Garcia-Rivera
Philippe A Gallay
Scripps Research Institute · US

Funding

Cyclophilins, Cyclophilin Inhibitors and Hepatitis CR01AI087746 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI GALLAY, PHILIPPE ANDRE · 2010 to 2014
$2.3M
Cyclophilins and the IFN ResponseR01AI105007 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI GALLAY, PHILIPPE ANDRE · 2014 to 2017
$1.6M
NIAID NIH HHS AI087746NIAID NIH HHS R01 AI087746NIAID NIH HHS R01 AI105007
6 · The paper itself

Abstract

The development of two distinct classes of hepatitis C antiviral agents, direct-acting antivirals (DAAs) and host-targeting antivirals (HTAs), have distinctly impacted the hepatitis C virus (HCV) field by generating higher sustained virological response (SVR) rates within infected patients, via reductions in both adverse side effects and duration of treatment when compared to the old standard of care. Today DAAs are actively incorporated into the standard of care and continue to receive the most advanced clinical trial analysis. With a multitude of innovative and potent second-generation DAA compounds currently being tested in clinical trials, it is clear that the future of DAAs looks very bright. In comparison to the other class of compounds, HTAs have been slightly less impactful, despite the fact that primary treatment regimens for HCV began with the use of an HTA - interferon alpha (IFNα). The compound was advantageous in that it provided a broad-reaching antiviral response; however deleterious side effects and viral/patient resistance has since made the compound outdated. HTA research has since moved onward to target a number of cellular host factors that are required for HCV viral entry and replication such as scavenger receptor-BI (SR-BI), 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCoA reductase), cyclophilin A (CypA), fatty acid synthase (FASN) and miRNA-122. The rationale behind pursuing these HTAs is based upon the extremely low mutational rate that occurs within eukaryotic cells, thereby creating a high genetic barrier to drug resistance for anti-HCV compounds, as well as pan-genotypic coverage to all HCV genotypes and serotypes. As the end appears near for HCV, it becomes important to ask if the development of novel HTAs should also be analyzed in combination with other DAAs, in order to address potential hard-to-treat HCV patient populations. Since the treatment regimens for HCV began with the use of a global HTA, could one end the field as well?

Indexed as

Antiviral AgentsClinical Trials as TopicDrug DiscoveryHepatitis C, ChronicHumansAntiviral AgentsAlisporivirCyclophilin AHCVHost-targeting antivirals

Identifiers

PMID24091203
PMCPMC3971122
OpenAlexW2075782647

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.