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Hepatitis B virus (HBV) antigens and DNA encompass the structural and genetic components of the virus that serve as primary targets and diagnostic markers in the management of chronic hepatitis B [4, 5]. These include the surface antigen (HBsAg), which is essential for viral entry; the envelope antigen (HBeAg), a marker of high replication; the core-related antigens (HBcrAg); and the viral DNA, which represents the circulating viral load [9, 11]. The presence and persistence of these factors are critical in the pathogenesis of HBV-related liver diseases, including chronic hepatitis, cirrhosis, and hepatocellular carcinoma [8, 15]. Modern therapeutic approaches target these components through various mechanisms: nucleos(t)ide analogues (NAs) inhibit the viral polymerase to suppress DNA synthesis, while novel antisense oligonucleotides (ASOs) and siRNAs are designed to degrade viral RNA and reduce the production of all viral proteins, aiming for a functional cure [3, 15]. Monitoring the quantitative levels of these antigens and DNA is the standard practice for evaluating treatment efficacy and determining the risk of disease progression or viral reactivation [1, 13].
Reverse transcriptase inhibition of viral polymerase, antisense-mediated degradation of viral RNA, RNA interference (siRNA), inhibition of viral entry via NTCP receptor binding, and immunomodulation through cytokine signaling.
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