| Literature DB >> 28709657 |
Julie Lucifora1, Anna Salvetti1, Xavier Marniquet2, Laurent Mailly3, Barbara Testoni1, Floriane Fusil4, Aurore Inchauspé5, Maud Michelet1, Marie-Louise Michel6, Massimo Levrero1, Pierre Cortez2, Thomas F Baumert7, François-Loic Cosset4, Cécile Challier2, Fabien Zoulim8, David Durantel9.
Abstract
Hepatitis B Virus (HBV) persists in infected hepatocytes as an episomal covalently-closed-circular DNA mini-chromosome, called cccDNA. As the main nuclear transcription template, HBV cccDNA is a key replication intermediate in the viral life cycle. Little is known about the mechanisms involved in its formation, maintenance and fate under antiviral therapies. This is mainly due to the lack of small immune-competent animal models able to recapitulate the entire HBV replication cycle, including formation of HBV cccDNA. Here we report that HBV cccDNA can be detected by Southern blot analyses in the liver of C57BL6 mice transduced with AAV-HBV. HBV cccDNA persists in the liver of these animals together with the AAV-HBV episome. We also set up a PCR strategy to distinguish the HBV cccDNA from the AAV-HBV episome. These suggest that the AAV-HBV/mouse model might be relevant to test drugs targeting HBV cccDNA regulation and persistence.Entities:
Keywords: Adeno-associated virus; Hepatitis B virus; Immune-competent mouse; Immune-therapeutics; cccDNA
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Year: 2017 PMID： 28709657 DOI： 10.1016/j.antiviral.2017.07.006
Source DB: PubMed Journal: Antiviral Res ISSN： 0166-3542 Impact factor: 5.970