Although not critical for hepatitis B virus (HBV) replication, splicing of HBV pre-genomic RNA generates multiple HBV splice variants, some of which have been shown to impact replication of the genome-length HBV on which they rely for their replication. To date, all replication studies of splice variants have utilised truncated RNA or over-expression constructs, and studies utilising constructs that produce authentic splice derived HBV RNA are lacking. Here we utilise a greater than genome length model to interrogate the complete replication phenotype of HBV splice variant Sp1, and investigate mechanisms by which it negatively impacts genome-length HBV replication.
All Keywords
【저자키워드】 Replication, splicing, Hepatitis B virus, core, SP1, HBx, precore,
【저자키워드】 Replication, splicing, Hepatitis B virus, core, SP1, HBx, precore,