Evidence map›Paper›PMID 24966582›Full record

ReviewWorld journal of gastroenterology2014

Pathogenesis and significance of hepatitis C virus steatosis: an update on survival strategy of a successful pathogen.

Amedeo Lonardo, Luigi Elio Adinolfi, Luciano Restivo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Therapeutic, preventive, and pathogenetic advances in viral hepatitis.Frontiers in cellular and infection microbiology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. [Emphasizing the mutual effects of metabolic-associated fatty liver disease with infectious disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
    Article
  13. Metabolic complications of hepatitis C virus infection.World journal of gastroenterology · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. Hepatitis C Virus: Viral Quasispecies and Genotypes.International journal of molecular sciences · 2017
    Review
  18. NAFLD: Is There Anything New under the Sun?International journal of molecular sciences · 2017
    Article
  19. Article
  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

8 authors at 1 institution in 1 country.

Amedeo LonardoAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
Luigi Elio AdinolfiAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
Luciano RestivoAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
Stefano BallestriAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
Dante RomagnoliAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
Enrica BaldelliAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
Fabio NascimbeniAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
Paola LoriaAmedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
University of Modena and Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) is a successful pathogen on the grounds that it exploits its host's metabolism to build up viral particles; moreover it favours its own survival by inducing chronic disease and the development of specific anatomic changes in the infected organ. Steatosis, therefore, is associated with HCV infection by necessity rather than by chance alone. Approximately 6% of HCV patients have steatohepatitis. Interestingly, HCV steatosis occurs in the setting of multiple metabolic abnormalities (hyperuricemia, reversible hypocholesterolemia, insulin resistance, arterial hypertension and expansion of visceral adipose tissue) collectively referred to as "hepatitis C-associated dysmetabolic syndrome" (HCADS). General, nonalcoholic fatty liver disease (NAFLD)-like, mechanisms of steatogenesis (including increased availability of lipogenic substrates and de novo lipogenesis; decreased oxidation of fatty substrates and export of fatty substrates) are shared by all HCV genotypes. However, genotype 3 seemingly amplifies such steatogenic molecular mechanisms reported to occur in NAFLD via more profound changes in microsomal triglyceride transfer protein; peroxisome proliferator-activated receptor alpha; sterol regulatory element-binding proteins and phosphatase and tensin homologue. HCV steatosis has a remarkable clinical impact in as much as it is an acknowledged risk factor for accelerated fibrogenesis; for impaired treatment response to interferon and ribavirin; and development of hepatocellular carcinoma. Recent data, moreover, suggest that HCV-steatosis contributes to premature atherogenesis via both direct and indirect mechanisms. In conclusion, HCV steatosis fulfills all expected requirements necessary to perpetuate the HCV life cycle. A better understanding of the physiology of HCADS will likely result in a more successful handling of disease with improved antiviral success rates.

Indexed as

AnimalsAntiviral AgentsAtherosclerosisCarcinoma, HepatocellularFatty LiverHepacivirusHepatitis CHost-Pathogen InteractionsHumansLipid MetabolismLiverLiver CirrhosisLiver NeoplasmsOxidative StressPrognosisRisk FactorsAntiviral AgentsAtherosclerosisFibrosisHepatitis C-associated dysmetabolic syndromeHepatitis C virusHepatocellular carcinomaSteatohepatitisSustained virological response

Identifiers

PMID24966582
PMCPMC4064057
OpenAlexW2026281421

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.