DECODING HEPATITIS B VIRUS: MOLECULAR INSIGHTS INTO VIRAL ARCHITECTURE, ENTRY PATHWAYS AND HOST DISEASE DYNAMICS.

Main Article Content

Khushdeep Singh
Sahiba Kukreja
Rajinderjit Singh Ahi
Sumit Kumar
Amandeep Singh Birdi
Kirti
Jaspreet Singh

Keywords

Hepatitis B virus (HBV), Viral genome organization, HBV surface and core antigens, NTCP receptor-mediated entry, Covalently closed circular DNA (cccDNA), HBV replication cycle, Host-virus interactions, Chronic hepatitis B progression, Hepatic fibrosis and cirrhosis, HBV-induced hepatocellular carcinoma (HCC).

Abstract

Background: Hepatitis B virus remains a significant global health concern, particularly in endemic regions such as Asia and Africa. Despite the availability of effective vaccines and antiviral therapies, chronic HBV infection continues to cause substantial morbidity and mortality through liver cirrhosis and hepatocellular carcinoma.


Aim: This review aims to provide a comprehensive understanding of the molecular architecture of HBV, its mechanisms of host entry, viral replication, and the progression to chronic liver disease. By decoding these processes, the study highlights potential avenues for improved therapeutic strategies.


Methods: A detailed literature-based analysis was conducted using peer-reviewed articles, molecular virology reports, and clinical studies focusing on HBV structure, genome organization, protein function, viral entry pathways, and the dynamics of host-pathogen interactions. The review integrates molecular data with clinical outcomes to elucidate how viral and host factors shape disease progression.


Key Findings: HBV has a compact, partially double-stranded DNA genome encoding four overlapping open reading frames, each critical for replication and immune evasion. Entry into hepatocytes is mediated by the NTCP, with subsequent formation of cccDNA serving as the key template for viral persistence.


Conclusion: Understanding the molecular and cellular mechanisms underpinning HBV infection is essential for developing more effective antiviral strategies. While current therapies can suppress viral replication, they do not eliminate cccDNA or fully reverse immune dysfunction in chronic carriers. Comprehensive insights into the viral life cycle and host responses provide a foundation for future therapeutic innovations.

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