Article ; Online: D
JHEP reports : innovation in hepatology
2020 Volume 3, Issue 1, Page(s) 100195
Abstract: Background & aims: Chronic HBV infection cannot be cured by current therapeutics owing to their limited ability to reduce covalently closed circular (ccc)DNA levels in the livers of infected individuals. Therefore, greater understanding of the molecular ...
Abstract | Background & aims: Chronic HBV infection cannot be cured by current therapeutics owing to their limited ability to reduce covalently closed circular (ccc)DNA levels in the livers of infected individuals. Therefore, greater understanding of the molecular determinants of cccDNA formation and persistence is required. One key issue is the extent to which Methods: We engineered an infectious HBV mutant with a genome encoding a stop codon at position T67 in the HBV core open reading frame (ΔHBc HBV). Importantly, ΔHBc HBV virions cannot initiate nucleocapsid synthesis upon infection. Long-term Results: ΔHBc and wild-type (WT) HBV resulted in comparable expression of HBV surface antigen (HBsAg), which could be blocked using the entry inhibitor Myrcludex B, confirming Conclusions: Our results imply that Lay summary: The hepatitis B virus can maintain itself in the liver for a patient's lifetime, causing liver injury and cancer. We have clarified exactly how it maintains itself in an infected cell. This now means we have a better idea at how to target the virus and cure a chronic infection. |
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Language | English |
Publishing date | 2020-10-14 |
Publishing country | Netherlands |
Document type | Journal Article |
ISSN | 2589-5559 |
ISSN (online) | 2589-5559 |
DOI | 10.1016/j.jhepr.2020.100195 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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