APOBEC3B edits HBV DNA and inhibits HBV replication during reverse transcription

Nonlytic Lymphocytes Engineered to Express Virus-Specific T-Cell Receptors Limit HBV Infection by Activating APOBEC3

“…This modality is masked on classical effector CD8 T cells that preferentially lyse their targets but is clearly detectable on RE-T cells that have low lytic contents. We propose that this feature, combined with the inability to activate liver inflammatory events, can be exploited for new therapeutic modalities for the treatment of persistent hepatic viral infections, in particular because induction of APOBEC3B activity in hepatocytes has been proposed as a strategy to inhibit HBV replication 29 and destabilize HBV cccDNA. 28 The direct antiviral efficacy of our TCR-reprogrammed RE-T cells in limiting HBV infection is quite remarkable.…”

“…Up-regulation of APOBEC3 cytidine deaminases A3A, A3B, and A3G through interferon alfa 27 and LTBR activation 28 have been shown to inhibit HBV replication by the induction of HBV-DNA hypermutations and might degrade cccDNA without causing hepatotoxicity. 28,29 Thus, we first quantified A3A, A3B, and A3G mRNA expression in HepG2.2.15 after 24 and 48 hours of treatment with RE-T cells, compared with IFN alfa or LTBR agonist (LTa1/b2) treatment ( Figure 4B and C). Treatment with RE-T cells (able to reduce intracellular HBV DNA by 31%) for 24 or 48 hours induced a 20%-40% increase in A3 and A3B relative mRNA, respectively, and a 450% increase in A3G relative mRNA ( Figure 4C).…”

Cyclin E2‐CDK2 mediates SAMHD1 phosphorylation to abrogate its restriction of HBV replication in hepatoma cells

“…Hepatitis B virus particle collection and infection with HepG2‐NTCP cells were conducted as described before . Briefly, HepG2‐NTCP cells were inoculated with concentrated HBV viral particles derived from supernatants of HepAD38 cells at 1000 genome equivalents (GE) per cell in the medium containing 5% PEG 8000 for 16 h, then the virus was removed from the infected cells and the cells were maintained in Williams’ E media before harvest.…”

Hepatitis B virus X protein modulates upregulation of DHX9 to promote viral DNA replication

“…For virus production and HBV infection, virus derived from the supernatant of HepAD38 cells (Ladner et al, 1997) was used for HBV infection. HepG2-NTCP cells were infected with HBV at 1000 genome equivalents (GE) per cell in the presence of 4% PEG8000 for 24 hr as described previously (Chen et al, 2018).…”

“…HBV DNA was isolated from intracellular core particles as described previously (Chen et al, 2018). Briefly, DNA in HBV core particles was collected through a sucrose density gradient and purified by proteinase K digestion and phenol/chloroform extraction.…”