Brief Report - (2023) Volume 7, Issue 2
Received: 29-May-2023, Manuscript No. rtr-23-113211;
Editor assigned: 31-May-2023, Pre QC No. P-113211;
Reviewed: 14-Jun-2023, QC No. Q-113211;
Revised: 19-Jun-2023, Manuscript No. R-113211;
Published:
26-Jun-2023
, DOI: 10.37421/2684-4273.2023.7.48
Citation: Liana, Ranella. “The Role of Hepatitis B and C in
Hepatocellular Carcinoma Development.” Rep Thyroid Res 7 (2023): 48.
Copyright: © 2023 Liana R. This is an open-access article distributed under the
terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author
and source are credited.
Hepatocellular Carcinoma (HCC) is one of the most prevalent and deadly forms of primary liver cancer worldwide. Its development is often associated with underlying chronic liver diseases, including Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) infections. This comprehensive review explores the intricate relationship between these two viruses and the development of HCC. We will delve into the epidemiology, pathogenesis, and molecular mechanisms linking HBV and HCV to HCC, as well as the clinical implications and prevention strategies for reducing the burden of HCC associated with viral hepatitis [1].
Hepatitis B Virus is a DNA virus transmitted through contact with infected blood or other body fluids. It is particularly endemic in regions such as sub- Saharan Africa and Southeast Asia, where vertical transmission from mother to child is a significant mode of infection. Chronic HBV infection increases the risk of HCC substantially, with a 15-25% lifetime risk of developing HCC in untreated individuals. Hepatitis C Virus is an RNA virus primarily transmitted through parenteral exposure to contaminated blood. HCV infection has a global distribution, with the highest prevalence in certain regions of Asia, Africa, and Eastern Europe. Chronic HCV infection is a leading cause of cirrhosis and HCC, with a 1-4% annual risk of HCC development in cirrhotic patients [2].
Both HBV and HCV can establish chronic infections in the liver, leading to sustained inflammation. This chronic inflammatory response contributes to hepatocyte damage and regeneration, creating an environment conducive to genetic mutations and cellular transformation. A significant proportion of chronic HBV and HCV infections progress to liver fibrosis and cirrhosis. Cirrhosis represents a key risk factor for HCC development, as it is characterized by extensive liver tissue remodeling, regenerating nodules, and an increased risk of genetic mutations and genomic instability. Integration of viral DNA or RNA into the host genome can occur during chronic infection. This integration can disrupt the host cell's DNA repair mechanisms and promote oncogenic events, ultimately leading to HCC. HBV and HCV have evolved multiple mechanisms to evade the host immune system, including modulation of antigen presentation and inhibition of immune cell function. Prolonged immune suppression contributes to the persistence of viral infection and the progression to HCC [3].
Integration of HBV DNA into the host genome can lead to the disruption of tumor suppressor genes and activation of oncogenes, contributing to HCC development. HBV produces proteins like HBx, which can directly promote hepatocyte proliferation, inhibit DNA repair, and induce genomic instability. The host immune response to HBV infection can lead to chronic inflammation and oxidative stress, which further drive HCC development. The progression of HCV-induced liver fibrosis to cirrhosis is a critical step in HCC development.
Cirrhosis-related tissue damage and regeneration create an environment conducive to malignant transformation. HCV core protein and non-structural proteins can interfere with cellular pathways involved in apoptosis and cell cycle regulation, contributing to oncogenesis. HCV infection can dysregulate host microRNAs, which play a role in gene expression control and may contribute to HCC development. HBV produces proteins like HBx, which can directly promote hepatocyte proliferation, inhibit DNA repair, and induce genomic instability. The host immune response to HBV infection can lead to chronic inflammation and oxidative stress, which further drive HCC development. The progression of HCVinduced liver fibrosis to cirrhosis is a critical step in HCC development. Cirrhosisrelated tissue damage and regeneration create an environment conducive to malignant transformation [4,5].
Hepatitis B and C viruses are significant contributors to the development of hepatocellular carcinoma, a highly lethal form of liver cancer. The interplay between chronic infection, inflammation, fibrosis, viral integration, and oncogenic protein expression creates an environment conducive to hepatocarcinogenesis. Understanding the molecular mechanisms involved and implementing effective prevention and management strategies are essential for reducing the burden of HCC associated with viral hepatitis. Vaccination, safe injection practices, early detection, and antiviral therapy play pivotal roles in this endeavor, offering hope for a future with fewer cases of hepatitis-related HCC.
None
None
Google Scholar, Crossref, Indexed at
Google Scholar, Crossref, Indexed at
Google Scholar, Crossref, Indexed at
Google Scholar, Crossref Indexed at
Reports in Thyroid Research received 4 citations as per Google Scholar report
