What is the intrinsic hepatocarcinogenic activity in hepatitis B (HBV) (Hep B) infection?

Updated: Jun 08, 2021
  • Author: Nikolaos T Pyrsopoulos, MD, PhD, MBA, FACP, AGAF; Chief Editor: BS Anand, MD  more...
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HBV has been speculated to have intrinsic hepatocarcinogenic activity, interacting with host DNA in different ways. After entering the hepatocyte, viral DNA is integrated within the genome. The site of integration is not constant but usually involves the terminal repeat sequences. Chromosomal deletions, translocations, rearrangements, inversions, or even duplications of normal DNA sequencing accompany integration.

Transactivation of the function of genes controlling transcriptional factors (ie, insulinlike growth factor II [IGF-2], transforming growth factor-alpha [TGF-a], TGF-beta, cyclin-a [a protein that controls cell division], epidermal growth factor-r [EGFR], retinoic acid receptor [RAR]), and oncogenes such as c-myc, fos, ras (activating the internal signal transduction cascade upregulating ras/mitogen–activated kinase, c-Jun N terminal kinase, nuclear factor–kB [NF-kB], Jak-1-STAT, src- dependent pathways) influence normal hepatocyte differentiation or cell cycle progression.

Furthermore, the integrated part of HBV controlling the production of the HBxAg (antigen for the X gene of HBV) is overexpressed. These observations suggest that the site of viral genomic integration into the host's DNA is not the only factor.

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