Deep mutational scanning of HBV reveals a mechanism for cis preferential reverse transcription

Hepatitis B virus (HBV) is a small double-stranded DNA virus that chronically infects 296 million people. Over half of its compact genome encodes protein in two overlapping reading frames, and during evolution, multiple selective pressures can act on shared nucleotides. This study combines an RNA-based HBV cell culture system with deep mutational scanning to uncouple cis- and trans-acting sequence requirements in the HBV genome. The results support a leaky ribosome scanning model for polymerase translation, provide a fitness map of the HBV polymerase at single nucleotide resolution, and identify conserved prolines adjacent to the HBV polymerase termination codon that stall ribosomes. Further experiments indicated that stalled ribosomes tether the nascent polymerase to its template RNA, ensuring cis-preferential RNA packaging and reverse transcription of the HBV genome., , , # Data from: Deep mutational scanning of HBV reveals a mechanism for cis preferential reverse transcription

[Access this dataset on Dryad](https://doi.org/10.5061/dryad.x3ffbg7qx)

The purpose of this dataset is to provide the analysis software, the raw pre-processed experimental data files, and the processed result files used in the paper “Deep mutational scanning of HBV reveals a mechanism for cis preferential reverse transcription”.

For detailed information on the experimental design, please refer to the paper. Briefly, mutants of the hepatitis B virus (HBV) were generated (input population) and transfected into cell cultures. In cell culture, HBV mutants were either depleted or enriched based on the effects of their mutations (output population). Afterwards, both input and output populations were sequenced to quantify the enrichment or depletion of each HBV mutant. From these sequencing results, so called codoncounts files were generated using barcoded-subamplicon sequencing softw...