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Hepatitis B virus (HBV) mRNA transcripts are the primary templates for the synthesis of viral proteins and the replication of the viral genome (Source: Liang, T. J., 2009, Hepatology). The HBV genome produces several distinct transcripts, including the 3.5kb pregenomic RNA (pgRNA), which serves as the template for reverse transcription, and subgenomic RNAs (2.4kb, 2.1kb, and 0.7kb) that encode the surface (HBsAg), core (HBcAg), polymerase, and X (HBx) proteins (Source: PubMed, PMID: 32635331). These transcripts are essential for maintaining the viral lifecycle and contributing to the persistence of chronic infection by overwhelming the host immune system with viral antigens (Source: PubMed, PMID: 31505302). Therapeutic strategies targeting these transcripts, such as antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs), aim to degrade the viral RNA, thereby reducing the production of all viral proteins and inhibiting viral replication (Source: Yuen et al., 2021, The Lancet Gastroenterology & Hepatology). This approach is intended to lower the HBsAg burden, potentially allowing for a functional cure by restoring the host's immune response against the virus (Source: Wooddell et al., 2017, Science Translational Medicine).
Degradation of viral mRNA via RNA interference (siRNA) or RNase H-mediated cleavage (antisense oligonucleotides) to inhibit viral protein synthesis and replication.
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