作者: Xiangyang Zu , Yang Liu , Shaobo Wang , Rui Jin , Zheng Zhou
DOI: 10.1016/J.ANTIVIRAL.2014.01.011
关键词: Peptide 、 Mutant 、 Virology 、 Viral entry 、 Glycoprotein 、 Viral envelope 、 Japanese encephalitis 、 Biology 、 Molecular biology 、 Virus 、 Receptor
摘要: Japanese encephalitis virus (JEV) is a major cause of acute viral in both humans and animals. Domain III the envelope glycoprotein (E DIII) plays an important role interaction particles with host cell receptors to facilitate entry. Intervention between E DIII its cognate receptor would provide avenue for inhibiting JEV infection. A phage display peptide library was therefore panned against DIII, which resulted identification several peptides. One peptide, named P3, inhibited infection BHK-21 cells IC₅₀ ∼1 μM IC₉₀ at ∼100 μM. Further characterization revealed that P3 bound K(d) 6.06 × 10⁻⁶ M by interfering attachment cells. Based on silico prediction ZDOCK, found interact via hydrophobic pocket, confirmed binding assay V357A mutant. hypothesized bind interacting sties adjacent BC DE loops, might interfere cellular receptors, thus impeding This newly isolated may represent new therapeutic candidate treatment JEV.