UAP56 is an essential factor in eukaryotic pre-mRNA splicing and mRNA export. Many viruses require cellular RNA export factors to efficiently export viral RNA. However, the mechanisms behind hepatitis B virus (HBV) RNA splicing and nuclear export remain poorly understood. Here, our data show that UAP56 interacts with the HBx protein. Moreover, we demonstrate that the Q-motif of UAP56, which regulates RNA-binding and helicase activity, is essential for the interaction of UAP56 with HBx. Both knockdown of UAP56 and deficiency of HBx impaired cytoplasmic accumulation of HBV RNA transcripts, whereas knockdown of UAP56 also reduced the level of HBV pregenomic RNA splicing variants. In addition, knockdown of Nxf1 induced HBV RNA nuclear accumulation. These findings provide unique insights into the mechanistic details of HBV RNA export and splicing.

UAP56是真核前mRNA剪接和mRNA输出中的重要因素。许多病毒需要细胞RNA输出因子才能有效输出病毒RNA。但是，对乙型肝炎病毒（HBV）RNA剪接和核输出的背后机制仍知之甚少。在这里，我们的数据表明UAP56与HBx蛋白相互作用。此外，我们证明了UAP56的Q基序调节RNA结合和解旋酶的活性，对于UAP56与HBx的相互作用至关重要。UAP56的敲低和HBx的缺乏都损害了HBV RNA转录物的细胞质积累，而UAP56的敲低也降低了HBV前基因组RNA剪接变体的水平。此外，敲低Nxf1诱导HBV RNA核积累。这些发现提供了对HBV RNA输出和剪接机制细节的独特见解。