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Introduction
Hepatitis B virus (HBV) infection poses a significant global health challenge, with an alarming estimate of approximately 290 million cases worldwide [1]. To combat this public health threat, international targets have been set for the elimination of HBV pollution by 2030 as part of the Sustainable Development Goals. Despite the magnitude of the problem, a substantial proportion of HBV infections remain undiagnosed and untreated, further exacerbating the burden of the disease [1, 2–3].
HBV is a small, partially double-stranded DNA virus belonging to the Hepadnaviridae family. It has a unique replication mechanism that involves the reverse transcription of an RNA intermediate, distinguishing it from other DNA viruses [4]. Structurally, HBV consists of an outer lipid envelope containing hepatitis B surface antigens (HBsAg) and an icosahedral nucleocapsid core, which encloses the viral genome and hepatitis B core antigen (HBcAg) [5]. The viral genome is approximately 3.2 kb in length and is organized into four partially overlapping open reading frames: S (encoding HBsAg), C (encoding HBcAg and hepatitis B e antigen [HBeAg]), P (encoding the viral polymerase responsible for DNA synthesis and reverse transcription), and X (encoding HBx protein, which plays a role in viral replication and oncogenesis) [6, 7]. The nucleocapsid protects the relaxed circular DNA (rcDNA), which is converted into covalently closed circular DNA (cccDNA) in the nucleus of infected hepatocytes, serving as a template for viral transcription and persistence [8]. Mutations within these genes can influence viral persistence, immune escape, and disease progression, contributing to HBV’s pathogenicity.
HBV is primarily transmitted through exposure to infected bodily fluids, such as blood, maternal-to-child transmission, sexual activity, and the use of shared intravenous drug equipment [9]. Chronic HBV infection, which lacks a known cure, carries a lifetime risk of 15–40% for complications including conditions like cirrhosis, liver failure, or hepatocellular carcinoma [10]. Beyond its direct impact on human health, HBV infection has exerted significant evolutionary pressure on human populations, influencing genetic susceptibility and immune system adaptations over time. Certain human leukocyte antigen (HLA) variants and immune response genes have been shaped by past exposures to HBV, reflecting the ongoing co-evolution between the virus and its hosts [11].
The high global burden of chronic HBV infection can also be viewed as a form of “viral pollution,” persistently...