Evidence map›Paper›PMID 25664450›Full record

ReviewBiomolecules2015

Hepatitis C, innate immunity and alcohol: friends or foes?

Natalia A Osna, Murali Ganesan, Kusum K Kharbanda

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Effects of alcohol consumption on viral hepatitis B and C.World journal of clinical cases · 2021
    Review
  6. Role of ALDH2 in Hepatic Disorders: Gene Polymorphism and Disease Pathogenesis.Journal of clinical and translational hepatology · 2021
    Review
  7. Second hits exacerbate alcohol-related organ damage: an update.Alcohol and alcoholism (Oxford, Oxfordshire) · 2021
    Review
  8. Review
  9. Article
  10. Acetaldehyde suppresses the display of HBV-MHC class I complexes on HBV-expressing hepatocytes.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Article
  11. Observational
  12. Article
  13. Role of apoptotic hepatocytes in HCV dissemination: regulation by acetaldehyde.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Article
  14. Pathogenesis of Alcohol-Associated Liver Disease.Journal of clinical and experimental hepatology
    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 at 1 institution in 1 country.

Natalia A OsnaResearch Service, Veterans Affairs Nebraska-Western Iowa Health Care System, 4101 Woolworth Ave, Omaha, NE 68105, USA. nosna@unmc.edu.
Murali GanesanResearch Service, Veterans Affairs Nebraska-Western Iowa Health Care System, 4101 Woolworth Ave, Omaha, NE 68105, USA. murali.ganesan@unmc.edu.
Kusum K KharbandaResearch Service, Veterans Affairs Nebraska-Western Iowa Health Care System, 4101 Woolworth Ave, Omaha, NE 68105, USA. kkharbanda@unmc.edu.
VA Nebraska Western Iowa Health Care System · US

Funding

Effect of Alcohol on Hepatic Creatine Biosynthesis: Role of Defective MethylationI01BX001155 · VA · OMAHA VA MEDICAL CENTER · PI KHARBANDA, KUSUM K. · 2012 to 2015
–
Ethanol-Induced Hypomethylation Accelerates Hepatitis C ProgressionI01BX001673 · VA · OMAHA VA MEDICAL CENTER · PI OSNA, NATALIA ALEKSANDR · 2013 to 2016
–
BLRD VA I01 BX001155BLRD VA I01 BX001673
6 · The paper itself

Abstract

Hepatitis C and alcohol are the most widespread causes of liver disease worldwide. Approximately 80% of patients with a history of hepatitis C and alcohol abuse develop chronic liver injury. Alcohol consumption in hepatitis C virus (HCV)-infected patients exacerbates liver disease leading to rapid progression of fibrosis, cirrhosis and even hepatocellular carcinoma. Hepatocytes are the main sites of HCV-infection and ethanol metabolism, both of which generate oxidative stress. Oxidative stress levels affect HCV replication and innate immunity, resulting in a greater susceptibility for HCV-infection and virus spread in the alcoholic patients. In this review paper, we analyze the effects of ethanol metabolism and other factors on HCV replication. In addition, we illustrate the mechanisms of how HCV hijacks innate immunity and how ethanol exposure regulates this process. We also clarify the effects of HCV and ethanol metabolism on interferon signaling-a crucial point for activation of anti-viral genes to protect cells from virus-and the role that HCV- and ethanol-induced impairments play in adaptive immunity which is necessary for recognition of virally-infected hepatocytes. In conclusion, ethanol exposure potentiates the suppressive effects of HCV on innate immunity, which activates viral spread in the liver and finally, leads to impairments in adaptive immunity. The dysregulation of immune response results in impaired elimination of HCV-infected cells, viral persistence, progressive liver damage and establishment of chronic infection that worsens the outcomes of chronic hepatitis C in alcoholic patients.

Indexed as

EthanolHepacivirusHumansImmunity, InnateLiverVirus ReplicationEthanol

Identifiers

PMID25664450
PMCPMC4384112
OpenAlexW2078318650

What OpenQuestion holds

Textmetadata
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.