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Hepatitis B surface antigen (HBsAg) and Hepatitis B e antigen (HBeAg) are essential viral proteins produced by the Hepatitis B virus (HBV) that play distinct roles in the viral life cycle and pathogenesis. HBsAg is a structural glycoprotein located on the viral envelope that facilitates attachment and entry into hepatocytes by interacting with the sodium taurocholate cotransporting polypeptide (NTCP) receptor (Liang, 2009). HBeAg is a secreted, non-structural protein that acts as a decoy and immunomodulator, promoting T-cell exhaustion and immune tolerance to ensure viral persistence (Seeger & Mason, 2015). In clinical practice, HBsAg is the primary diagnostic marker for infection, and its clearance is the gold standard for a functional cure, while HBeAg serves as a marker for high levels of viral replication (Irie et al., 2023). Therapeutic strategies targeting these antigens include antisense oligonucleotides and siRNAs that degrade viral mRNA to reduce antigen burden, as well as monoclonal antibodies designed to neutralize and clear circulating HBsAg (Yuen et al., 2021). By reducing the high levels of these antigens, these therapies aim to alleviate immune suppression and allow the host's immune system to regain control over the infection.
RNA interference-mediated mRNA degradation, antisense oligonucleotide-mediated mRNA cleavage, monoclonal antibody-mediated neutralization and clearance, and vaccine-induced active immunization.
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