Division of Avian Infectious Diseases, National State Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 427 Maduan Street, Nangang District, Harbin 150001, PR China.
Vaccine. 2010 May 7;28(21):3735-40. doi: 10.1016/j.vaccine.2010.02.102. Epub 2010 Mar 20.
A mutant infectious bursal disease virus (IBDV) deficient in expressing VP5, rGx-F9VP2DeltaVP5, was generated using reverse genetics technology. In comparison to the characteristics of rGx-F9VP2 virus in vitro, the mutant virus demonstrated lower viral titer and cytopathogenicity. To understand the role of VP5 in the pathogenicity of IBDV in vivo, animal experiments were conducted. rGx-F9VP2DeltaVP5 caused reduced bursal lesion of SPF chickens compared to rGx-F9VP2. Although rGx-F9VP2DeltaVP5 induced lower serum antibody than rGx-F9VP2 did, both inoculated groups were fully protected against vvIBDV challenge 4 weeks post-inoculation. In addition, immunosuppression induced by VP5-deficient virus was studied in 2-week-old SPF chickens immunized with AIV inactivated vaccine. And there was reduced immunosuppression as shown in our experimental results. The results showed that AIV hemagglutination inhibition (HI) antibodies of the rGx-F9VP2DeltaVP5 inoculated group were similar to those of the mock-inoculated group, however, they were higher than those of the rGx-F9VP2 inoculated group, indicating that deficiency of VP5 decreased the immunosuppression of rGx-F9VP2DeltaVP5 in chickens. All data indicated that VP5 played an important role in viral replication and pathogenesis both in vitro and in vivo. The VP5-deficient mutant virus could be a good candidate as a marked vaccine.
一株缺失 VP5 基因表达的传染性法氏囊病病毒（IBDV）突变株 rGx-F9VP2DeltaVP5 通过反向遗传技术构建。与 rGx-F9VP2 病毒的体外特性相比，该突变病毒的病毒滴度和细胞病变效应较低。为了研究 VP5 在 IBDV 体内致病性中的作用，进行了动物实验。与 rGx-F9VP2 相比，rGx-F9VP2DeltaVP5 引起 SPF 鸡法氏囊病变减轻。尽管 rGx-F9VP2DeltaVP5 诱导的血清抗体水平低于 rGx-F9VP2，但接种两组均在接种后 4 周完全免受 vvIBDV 攻毒。此外，在 2 周龄 SPF 鸡中研究了 VP5 缺失病毒引起的免疫抑制作用，这些鸡用 AIV 灭活疫苗免疫。实验结果表明，VP5 缺失病毒引起的免疫抑制作用降低。结果表明，rGx-F9VP2DeltaVP5 接种组的 AIV 血凝抑制（HI）抗体与模拟接种组相似，但高于 rGx-F9VP2 接种组，表明 VP5 缺失降低了 rGx-F9VP2DeltaVP5 在鸡中的免疫抑制作用。所有数据表明，VP5 在体外和体内均对病毒复制和致病性起重要作用。VP5 缺失突变株可能是一种良好的标记疫苗候选株。
