Analysis of the infection mechanism of human hepatitis B virus using bio-nanocapsule.

利用新型的酵母源乙肝表面抗原L颗粒作为非感染性亚病毒颗粒，研究了乙肝病毒的感染机制，特别是尚未解决的膜融合机制。我们成功地在乙型肝炎表面抗原L蛋白的N端发现了一个新的膜融合基序。我们还证明了疏水的苯丙氨酸残基(Phe13和Phe14)是这种融合活性所必需的。

By using novel yeast-derived HBsAg L particles, named bio-nanocapsules (BNC), as noninfectious subviral particles, we studied the infectious mechanisms, especially the membrane fusion mechanism that remain unsolved, of HBV. We successfully identified a novel membrane fusion motif located at the N-terminal region of HBsAg L protein. We also demonstrated that the hydrophobic phenylalanine residues (Phe13 and Phe14) were essential for this fusion activity.