Article Per Year (5 Year)
p-Index From 2020 - 2025
0.408
P-Index
This Author published in this journals
All Journal Genbinesia Journal of Biology
Sima, Putri Melati
Unknown Affiliation
Agriculture, Biological Sciences & Forestry Biochemistry, Genetics & Molecular Biology Chemical Engineering, Chemistry & Bioengineering Health Professions Immunology & microbiology

Published : 1 Documents Claim Missing Document
Claim Missing Document
Check
Articles

Found 1 Documents
Search

 1 
Molecular Mechanisms of Hepatitis C Virus (HCV) Triggering Normal Cell Transformation into Cancer: A Mini Review Dhea Kharisma, Viol; Sima, Putri Melati
Genbinesia Journal of Biology Vol. 2 No. 3 (2023): July 2023
Publisher : Generasi Biologi Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.55655/genbinesia.v2i3.43

Abstract

Hepatitis C virus (HCV) infection has become a serious concern because it can trigger the severity of complications leading to hepatocellular carcinoma (HCC). HCV is a virus with single-stranded RNA (ssRNA) type genetic material, with virions composed of structural proteins such as glycoprotein, envelope, and core, then HCV also has nonstructural proteins such as NS3, NS4, NS4B, NS5A, NS5B. The development of HCV infection therapy has been carried out through direct-acting antiviral agents (DAAs) with the hope of achieving a reduction in mortality and HCC risk. However, these strategies cannot fully reduce the risk of HCC in patients who have recovered from HCV infection. This review briefly reviews several factors from the virus and host to trigger cellular transformation of hepatocytes into HCC. HCV infection can trigger the transformation of hepatocytes into cancer in the case of HCC influenced by two factors consisting of pro-oncogenic and growth factors. Pro-oncogenic of HCV initiates HCC through the release of ROS that triggers genetic mutations and upregulation of proliferation in hepatocytes, it allows internal cell factors to also work in the process of transformation into cancer such as increased growth factor activity for antiapoptotic response, survival, and proliferation to trigger increased severity of HCC.
Co-Authors Dhea Kharisma, Viol