Abstract
BackgroundThe effects of Hepatitis B virus (HBV) rtA181T/sW172* mutation on viral replication and pathogenicity was concerned recently. This study aimed to investigate the biological characteristics of rtA181T/sW172* mutant strain of HBV in animal model.MethodsThe rtA181T/sW172* mutant plasmid was constructed using the pHBV4.1 (wild type HBV) as a template. The wild and mutant HBV replication mouse models were established utilizing a hydrodynamic technique. The titers of hepatitis B surface antigen (HBsAg), hepatitis B e antigen, and HBV DNA in serum, and the levels of HBsAg, hepatitis B core antigen(HBcAg), HBV DNA replication intermediates (HBV DNA RI) and HBV RNA in liver were measured after 1, 3, 5, 7, 10, 12 and 15 days of plasmid injection.ResultsIn wild-type HBV replication mouse model, serum HBsAg was high on day 1, 3, and 5, but became lower since day 7; while in mutant HBV mouse model, serum HBsAg was always at very low level. In liver tissues, HBV DNA RI of wild type HBV was detected on day 1 after transfection. The level subsequently peaked on day 3, gradually declined after day 5, and was almost undetectable on day 10. However, the HBV DNA RI levels of the mutant strain were always higher and lasted longer until day 15. Consistently, the expression levels of HBsAg and HBcAg in liver of the mutant group were significantly increased.ConclusionsIn the case of the HBV rtA181T/sW172* mutation, the secretion of serum HBsAg was impaired, whereas HBV DNA replication and HBsAg/HBcAg expression were increased in liver. These results suggest that the mutation can impair HBsAg secretion, and may cause the accumulation of viral core particles in liver.
Highlights
The effects of Hepatitis B virus (HBV) rtA181T/sW172* mutation on viral replication and pathogenicity was concerned recently
In the case of the HBV rtA181T/sW172* mutation, the secretion of serum hepatitis B surface antigen (HBsAg) was impaired, whereas HBV DNA replication and HBsAg/Hepatitis B core antigen (HBcAg) expression were increased in liver
These results suggest that the mutation can impair HBsAg secretion, and may cause the accumulation of viral core particles in liver
Summary
The effects of Hepatitis B virus (HBV) rtA181T/sW172* mutation on viral replication and pathogenicity was concerned recently. There are currently two classes of antiviral agents for chronic hepatitis B (CHB): nucleos(t) ide analogs (NAs) directly inhibiting HBV DNA replication and interferon-based therapies that may modulate the host immune response as well as viral replication. HBV DNA has a very compact coding organization with four partially overlapping open reading frames (ORFs), including ORF P, X, S and C [2]. The HBV surface proteins, including the S protein (226 amino acids), the M protein (281 amino acids), and the L protein (389–400 amino acids), are encoded by one long open reading frame that utilizes three different start codons and the same stop codon
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
