HBV Infection and Host Interactions: The Role in Viral Persistence and Oncogenesis

Abstract

Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve. Complex interactions between virus and host are responsible for HBV persistence and the risk of oncogenesis. Through multiple pathways, HBV is able to silence both innate and adaptive immunological responses and become out of control. Furthermore, the integration of the viral genome into that of the host and the production of covalently closed circular DNA (cccDNA) represent reservoirs of viral persistence and account for the difficult eradication of the infection. An adequate knowledge of the virus–host interaction mechanisms responsible for viral persistence and the risk of hepatocarcinogenesis is necessary for the development of functional cures for chronic HBV infection. The purpose of this review is, therefore, to analyze how interactions between HBV and host concur in the mechanisms of infection, persistence, and oncogenesis and what are the implications and the therapeutic perspectives that follow.

Identification of Cholangiocarcinoma (CCA) Subtype-Specific Biomarkers

“…This discovery is consistent with the transcription profiling data reported in various cancer types [30][31][32][33][34], including HCC [31,35]. Recognizing the significant role of TFs in the progression of liver cancers [38][39][40][41][42], we conducted enrichment analyses to unveil the signaling pathways in which the identified TFs are implicated in the context of CCA. By utilizing three enrichment libraries (GO, KEGG, DOSE), our analyses were directed towards the identification of CCA-specific TFs with potential as prognostic biomarkers (Suppl.…”

“…Numerous new prognostic biomarkers or biomarker combinations derived from TFs have been identified through comprehensive omics analyses of transcription profiles across different cancer types [30][31][32][33][34], including HCC [31,35]. As numerous cases of liver cancer arise from chronic health conditions like cirrhosis triggered by hepatitis B or hepatitis C infections [18][19][20]22,23,[36][37][38], alterations in gene expression induced by viruses have been documented at both the DNA and RNA levels [38][39][40][41][42]. This underscores the importance of TFs participating in the development of liver cancers.…”

Hepatitis B in Pediatric Population: Observational Retrospective Study in Romania

“…In young immune-tolerant individuals, a significant HBV-specific T cell response activity is demonstrated; thus, the idea that children infected at birth or in early childhood will remain in an immune-tolerant state with no disease or minimal disease for at least 10 years is considered to be improbable nowadays [ 58 , 59 ]. Even inactive carriers may be at risk for HCC because of HBV DNA integration in the host genome, which can occur in all stages of the disease, starting from the very first days of infection [ 60 ].…”

Ligand-based pharmacophore modeling, virtual screening, and 2D quantitative structure-activity relationship performance on anti-Hepatitis B virus flavonols

“…The global health impact is significant, affecting more than 300 million individuals with chronic HBV (CHB) [3] infections and causing approximately 820,000 deaths each year from complications such as cirrhosis and hepatocellular carcinoma [4]. One major obstacle presented by HBV is its ability to persist in the hepatocytes of the host, which can result in the development of chronic infection from an initial acute infection [5][6][7][8][9]. It is also associated with miscarriage and premature birth in pregnant women who are infected [10,11].…”