AI Article Synopsis
- Hepatitis Delta virus (HDV) depends on Hepatitis B virus and has a unique RNA genome that relies on host cell machinery for replication.
- S-HDAg, a protein associated with HDV, interacts with the BAZ2B protein to promote HDV RNA synthesis and replication.
- Disruption of S-HDAg or BAZ2B function significantly hinders HDV replication, indicating a crucial interaction essential for the virus's life cycle.
Article Abstract
Hepatitis Delta virus (HDV) is a satellite of Hepatitis B virus with a single-stranded circular RNA genome. HDV RNA genome synthesis is carried out in infected cells by cellular RNA polymerases with the assistance of the small hepatitis delta antigen (S-HDAg). Here we show that S-HDAg binds the bromodomain (BRD) adjacent to zinc finger domain 2B (BAZ2B) protein, a regulatory subunit of BAZ2B-associated remodeling factor (BRF) ISWI chromatin remodeling complexes. shRNA-mediated silencing of BAZ2B or its inactivation with the BAZ2B BRD inhibitor GSK2801 impairs HDV replication in HDV-infected human hepatocytes. S-HDAg contains a short linear interacting motif (SLiM) KacXXR, similar to the one recognized by BAZ2B BRD in histone H3. We found that the integrity of the S-HDAg SLiM sequence is required for S-HDAg interaction with BAZ2B BRD and for HDV RNA replication. Our results suggest that S-HDAg uses a histone mimicry strategy to co-activate the RNA polymerase II-dependent synthesis of HDV RNA and sustain HDV replication.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6972770 | PMC |
| http://dx.doi.org/10.1038/s41467-020-14299-9 | DOI Listing |
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