传染性法氏囊病病毒分子结构与功能研究进展

Progress in Relation of Molecular Structure and Function of Infectious Bursal Disease Virus

本文对传染性法氏囊病病毒的分子结构与功能的关系及致病的分子基础作了综述。 IBDV的主要保护性抗原及抗原表位的变异位于结构蛋白 VP2上。病毒多肽成熟需经二次切割 ,NCR可影响病毒的转录和 /或翻译 ,VP1 - VP3复合体的形成是 IBDV装配的重要环节。不同毒力型的 IBDV的出现除与基因突变、重组、重排有关 ,还可能与 VP5有关 ,也证实了 NCR与血清型的致病性无关。

The major protective antigen and variable antigen epitopes were located on VP2 of infectious bursal disease virus (IBDV).A two step cleavage processing of polypeptides for maturation of virus was found Noncoding regions(NCRs) may influence transcription and/or translation of IBDV.Formation VP1 VP3 complexes is likely to be a key step for the morphogenesis of IBDV particles.Genetic mutation,recombinant and reassortment may play an important role in emergence of different virulent IBDV,so does nonstructural protein VP5.The NCRs of segment A are not responsible for the different pathotypes of IBDV serotypes Ⅰand Ⅱ.