Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma

Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. Solid...

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Published inWorld journal of gastroenterology : WJG Vol. 26; no. 38; pp. 5759 - 5783
Main Authors D'souza, Simmone, Lau, Keith CK, Coffin, Carla S, Patel, Trushar R
Format Journal Article
LanguageEnglish
Published United States Baishideng Publishing Group Inc 14.10.2020
Subjects
Carcinoma, Hepatocellular
Hepatitis B - complications
Hepatitis B virus - genetics
Hepatitis, Viral, Human
Humans
Liver Neoplasms
Review
Hallmarks of cancer
Viral hepatitis
Hepatitis delta virus co-infection
Molecular mechanisms
Hepatocellular carcinoma
Hepatitis B virus
Hepatitis C virus
Chronic viral infection
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Abstract Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. Solid tumors like HCC are complex and have heterogeneous tumor genomic profiles contributing to complexity in diagnosis and management. Chronic infection with hepatitis B virus (HBV), hepatitis delta virus (HDV), and hepatitis C virus (HCV) are the greatest etiological risk factors for HCC. Due to the significant role of chronic viral infection in HCC development, it is important to investigate direct (viral associated) and indirect (immune-associated) mechanisms involved in the pathogenesis of HCC. Common mechanisms used by HBV, HCV, and HDV that drive hepatocarcinogenesis include persistent liver inflammation with an impaired antiviral immune response, immune and viral protein-mediated oxidative stress, and deregulation of cellular signaling pathways by viral proteins. DNA integration to promote genome instability is a feature of HBV infection, and metabolic reprogramming leading to steatosis is driven by HCV infection. The current review aims to provide a brief overview of HBV, HCV and HDV molecular biology, and highlight specific viral-associated oncogenic mechanisms and common molecular pathways deregulated in HCC, and current as well as emerging treatments for HCC.
AbstractList Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. Solid tumors like HCC are complex and have heterogeneous tumor genomic profiles contributing to complexity in diagnosis and management. Chronic infection with hepatitis B virus (HBV), hepatitis delta virus (HDV), and hepatitis C virus (HCV) are the greatest etiological risk factors for HCC. Due to the significant role of chronic viral infection in HCC development, it is important to investigate direct (viral associated) and indirect (immune-associated) mechanisms involved in the pathogenesis of HCC. Common mechanisms used by HBV, HCV, and HDV that drive hepatocarcinogenesis include persistent liver inflammation with an impaired antiviral immune response, immune and viral protein-mediated oxidative stress, and deregulation of cellular signaling pathways by viral proteins. DNA integration to promote genome instability is a feature of HBV infection, and metabolic reprogramming leading to steatosis is driven by HCV infection. The current review aims to provide a brief overview of HBV, HCV and HDV molecular biology, and highlight specific viral-associated oncogenic mechanisms and common molecular pathways deregulated in HCC, and current as well as emerging treatments for HCC.Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. Solid tumors like HCC are complex and have heterogeneous tumor genomic profiles contributing to complexity in diagnosis and management. Chronic infection with hepatitis B virus (HBV), hepatitis delta virus (HDV), and hepatitis C virus (HCV) are the greatest etiological risk factors for HCC. Due to the significant role of chronic viral infection in HCC development, it is important to investigate direct (viral associated) and indirect (immune-associated) mechanisms involved in the pathogenesis of HCC. Common mechanisms used by HBV, HCV, and HDV that drive hepatocarcinogenesis include persistent liver inflammation with an impaired antiviral immune response, immune and viral protein-mediated oxidative stress, and deregulation of cellular signaling pathways by viral proteins. DNA integration to promote genome instability is a feature of HBV infection, and metabolic reprogramming leading to steatosis is driven by HCV infection. The current review aims to provide a brief overview of HBV, HCV and HDV molecular biology, and highlight specific viral-associated oncogenic mechanisms and common molecular pathways deregulated in HCC, and current as well as emerging treatments for HCC.
Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. Solid tumors like HCC are complex and have heterogeneous tumor genomic profiles contributing to complexity in diagnosis and management. Chronic infection with hepatitis B virus (HBV), hepatitis delta virus (HDV), and hepatitis C virus (HCV) are the greatest etiological risk factors for HCC. Due to the significant role of chronic viral infection in HCC development, it is important to investigate direct (viral associated) and indirect (immune-associated) mechanisms involved in the pathogenesis of HCC. Common mechanisms used by HBV, HCV, and HDV that drive hepatocarcinogenesis include persistent liver inflammation with an impaired antiviral immune response, immune and viral protein-mediated oxidative stress, and deregulation of cellular signaling pathways by viral proteins. DNA integration to promote genome instability is a feature of HBV infection, and metabolic reprogramming leading to steatosis is driven by HCV infection. The current review aims to provide a brief overview of HBV, HCV and HDV molecular biology, and highlight specific viral-associated oncogenic mechanisms and common molecular pathways deregulated in HCC, and current as well as emerging treatments for HCC.
Author Patel, Trushar R
D'souza, Simmone
Lau, Keith CK
Coffin, Carla S
Author_xml – sequence: 1
  givenname: Simmone
  surname: D'souza
  fullname: D'souza, Simmone
– sequence: 2
  givenname: Keith CK
  surname: Lau
  fullname: Lau, Keith CK
– sequence: 3
  givenname: Carla S
  surname: Coffin
  fullname: Coffin, Carla S
– sequence: 4
  givenname: Trushar R
  surname: Patel
  fullname: Patel, Trushar R
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33132633$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved. 2020
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Issue 38
Keywords Hallmarks of cancer
Viral hepatitis
Hepatitis delta virus co-infection
Molecular mechanisms
Hepatocellular carcinoma
Hepatitis B virus
Hepatitis C virus
Chronic viral infection
Language English
License The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
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Supported by Canada Research Chair Program; Alberta Innovates Strategic Research Projects, No. G2018000880; and Calgary Clinical Research Fund Pilot, No. CRF18-0704.
Author contributions: D’souza S wrote the article; Lau KCK, Coffin CS, Patel TR, formatted and revised the article.
Corresponding author: Trushar R Patel, PhD, Associate Professor, Department of Chemistry and Biochemistry, Alberta RNA Research and Training Institute, University of Lethbridge, 4401 University Drive West, Lethbridge T1K3M4, AB, Canada. trushar.patel@uleth.ca
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Snippet Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the...
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SubjectTerms Carcinoma, Hepatocellular
Hepatitis B - complications
Hepatitis B virus - genetics
Hepatitis, Viral, Human
Humans
Liver Neoplasms
Review
Title Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma
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