For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
Inviting an author to review:
Green methods of lignocellulose pretreatment for biorefinery development
Find an author and click ‘Invite to review selected article’ near their name.
Search for authorsSearch for similar articles
24
views
75
references
 Top references
cited by
27
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      671
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The oncogenic role of hepatitis delta virus in hepatocellular carcinoma

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Summary

          Hepatitis delta virus (HDV) is a small defective virus that needs hepatitis B virus (HBV) to replicate and propagate. HDV infection affects 20-40 million people worldwide and pegylated interferon (PegIFN) is the only recommended therapy. There is limited data on the contribution of HDV infection to HBV-related liver disease or liver cancer. Evidence from retrospective and cohort studies suggests that HBV/HDV coinfection accelerates progression to cirrhosis and is associated with an increased risk of hepatocellular carcinoma (HCC) development compared to HBV monoinfection. Although the life cycle of HDV is relatively well known, there is only ancillary information on the molecular mechanisms that can drive specific HDV-related oncogenesis. No thorough reports on the specific landscape of mutations or molecular classes of HDV-related HCC have been published. This information could be critical to better understand the uniqueness, if any, of HDV-related HCC and help identify novel targetable mutations. Herein, we review the evidence supporting an oncogenic role of HDV, the main reported mechanisms of HDV involvement and their impact on HCC development.

          Graphical abstract

          Related collections

          Most cited references75

          • Record: found
          • Abstract: found
          • Article: not found

          DNA methylation-based prognosis and epidrivers in hepatocellular carcinoma.

          Augusto Villanueva, Anna Portela, Sergi Sayols … (2015)
          Epigenetic deregulation has emerged as a driver in human malignancies. There is no clear understanding of the epigenetic alterations in hepatocellular carcinoma (HCC) and of the potential role of DNA methylation markers as prognostic biomarkers. Analysis of tumor tissue from 304 patients with HCC treated with surgical resection allowed us to generate a methylation-based prognostic signature using a training-validation scheme. Methylome profiling was done with the Illumina HumanMethylation450 array (Illumina, Inc., San Diego, CA), which covers 96% of known cytosine-phosphate-guanine (CpG) islands and 485,000 CpG, and transcriptome profiling was performed with Affymetrix Human Genome U219 Plate (Affymetrix, Inc., Santa Clara, CA) and miRNA Chip 2.0. Random survival forests enabled us to generate a methylation signature based on 36 methylation probes. We computed a risk score of mortality for each individual that accurately discriminated patient survival both in the training (221 patients; 47% hepatitis C-related HCC) and validation sets (n = 83; 47% alcohol-related HCC). This signature correlated with known predictors of poor outcome and retained independent prognostic capacity of survival along with multinodularity and platelet count. The subset of patients identified by this signature was enriched in the molecular subclass of proliferation with progenitor cell features. The study confirmed a high prevalence of genes known to be deregulated by aberrant methylation in HCC (e.g., Ras association [RalGDS/AF-6] domain family member 1, insulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g., NOTCH3) and describes potential candidate epidrivers (e.g., septin 9 and ephrin B2).
          Article 0 comments Cited 187 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The hepatitis delta virus: Replication and pathogenesis.

            Camille Sureau, Francesco Negro (2016)
            Hepatitis delta virus (HDV) is a defective virus and a satellite of the hepatitis B virus (HBV). Its RNA genome is unique among animal viruses, but it shares common features with some plant viroids, including a replication mechanism that uses a host RNA polymerase. In infected cells, HDV genome replication and formation of a nucleocapsid-like ribonucleoprotein (RNP) are independent of HBV. But the RNP cannot exit, and therefore propagate, in the absence of HBV, as the latter supplies the propagation mechanism, from coating the HDV RNP with the HBV envelope proteins for cell egress to delivery of the HDV virions to the human hepatocyte target. HDV is therefore an obligate satellite of HBV; it infects humans either concomitantly with HBV or after HBV infection. HDV affects an estimated 15 to 20 million individuals worldwide, and the clinical significance of HDV infection is more severe forms of viral hepatitis--acute or chronic--, and a higher risk of developing cirrhosis and hepatocellular carcinoma in comparison to HBV monoinfection. This review covers molecular aspects of HDV replication cycle, including its interaction with the helper HBV and the pathogenesis of infection in humans.
            Article 0 comments Cited 97 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A 28-year study of the course of hepatitis Delta infection: a risk factor for cirrhosis and hepatocellular carcinoma.

              Angelo Sangiovanni, Roberto De Masi, Raffaella Romeo … (2009)
              Chronic infection with hepatitis Delta virus (HDV) is a risk factor for cirrhosis and hepatocellular carcinoma (HCC); predictors of disease outcome are, however, poorly defined. We tracked the course of HDV infection in 299 patients over a mean period of 233 months. We analyzed data from patients who had been HDV positive for at least 6 months (230 males; mean age, 30 years) admitted from 1978 to 2006 to Maggiore Hospital, Milan. HDV infection was defined by the presence of HDV antigen in liver tissue or serum HDV RNA in anti-HDV/hepatitis B surface antigen seropositive patients. At enrollment, 7 patients had acute hepatitis, 101 had mild-moderate chronic hepatitis, 76 had severe chronic hepatitis, and 104 had histologic or clinical cirrhosis. Ninety patients were treated with interferon, 62 with corticosteroids, and 12 with nucleoside analogues; 135 received no therapy. Over a mean period of 233 months, 82 patients developed cirrhosis. Among the 186 total patients with cirrhosis, 46 developed HCC, 43 ascites, 44 jaundice, and 1 encephalopathy. Female sex, alcohol abuse, and HDV replication were associated with liver decompensation; HBV replication and interferon were associated with HCC development. By the end of the study, 186 patients were still alive, 63 had died, and 29 had received liver transplants. The main cause of death was liver failure (n = 37, 59%); HDV replication was the only independent predictor of mortality. Persistent HDV replication leads to cirrhosis and HCC at annual rates of 4% and 2.8%, respectively, and is the only predictor of liver-related mortality.
              Article 0 comments Cited 83 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Augusto Villanueva
                Josep M. Llovet
                Journal
                Journal ID (nlm-ta): JHEP Rep
                Journal ID (iso-abbrev): JHEP Rep
                Title: JHEP Reports
                Publisher: Elsevier
                ISSN (Electronic): 2589-5559
                Publication date PMC-release: 16 May 2019
                Publication date Collection: August 2019
                Publication date (Electronic): 16 May 2019
                Volume: 1
                Issue: 2
                Pages: 120-130
                Affiliations
                [1 ]Mount Sinai Liver Cancer Program, Division of Liver Diseases, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA
                [2 ]Hepatology Section, Gastroenterology Department, Hospital del Mar, IMIM, Universitat Autònoma de Barcelona, Barcelona, Catalonia, Spain
                [3 ]Division of Hematology and Medical Oncology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, USA
                [4 ]Translational Research in Hepatic Oncology, Liver Unit, IDIBAPS, CIBERehd, Hospital Clínic, University of Barcelona, Barcelona, Catalonia, Spain
                [5 ]Institució Catalana de Recerca i Estudis Avançats, Barcelona, Catalonia, Spain
                [6 ]Denotes co-senior authorship.
                Author notes
                [* ]Corresponding authors. Addresses: Mount Sinai Liver Cancer Program, Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, 1425 Madison Avenue, Box 11-23, New York, NY 10029, USA; Tel.: +1 2126599503, fax: +1 212 849 2574, (JM. Llovet); or Division of Liver Diseases, Division of Hematology and Medical Oncology, Department of Medicine, Liver Cancer Program, Tisch Cancer Institute, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029 USA (A. Villanueva). augusto.villanueva@ 123456mssm.edu josep.llovet@ 123456mountsinai.org
                [†]

                These authors contributed equally to this work.

                Article
                Publisher ID: S2589-5559(19)30034-5
                DOI: 10.1016/j.jhepr.2019.05.001
                PMC ID: 7001537
                PubMed ID: 32039360
                SO-VID: f8b78672-c420-4be7-82b8-21dde0c60c7c
                Copyright © © 2019 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 17 February 2019
                Date revision received : 18 April 2019
                Date accepted : 5 May 2019
                Categories
                Subject: Review

                Keywords: hepatitis b virus,liver cancer,hcc, co-infection,molecular pathogenesis,defective,superinfection
                Data availability:
                Keywords: hepatitis b virus, liver cancer, hcc, co-infection, molecular pathogenesis, defective, superinfection

                Comments

                Comment on this article

                scite_

                Similar content671

                See all similar

                Cited by27

                See all cited by

                Most referenced authors3,604

                See all reference authors