Food Animal Health Research Program, Department of Veterinary Preventive Medicine, Ohio Agricultural Research and Development Center, The Ohio State University, 1680 Madison Avenue, Wooster, OH 44691, USA.
Virology. 2011 Jan 5;409(1):33-7. doi: 10.1016/j.virol.2010.09.030. Epub 2010 Oct 20.
We examined the effect of amino acids 222 and 254 on antigenicity of the variant Del-E strain of infectious bursal disease virus (IBDV). Using molecular epidemiology, we identified a virus designated as Del-E-222 that was identical to Del-E except for alanine at position 222. A second virus was generated using reverse genetics of the Del-E backbone to create Del-E-254 that contained an asparagine at amino acid 254. The Del-E-222 and Del-E-254 viruses were tested for their ability to escape neutralizing immunity provided by parenteral vaccination. The bursas from birds vaccinated with parental Del-E and challenged with Del-E-222 or Del-E-254 had macroscopic lesions typical of an IBDV infection, and their B-BW ratios were significantly smaller than the controls. Microscopic lesions included lymphocyte depletion and confirmed the ability of Del-E-222 and Del-E-254 to break through the immunity induced by the parental Del-E virus vaccination. Both mutations appear to be contributing to antigenic drift.
我们研究了氨基酸 222 和 254 对传染性法氏囊病病毒(IBDV)变异 Del-E 株抗原性的影响。利用分子流行病学,我们鉴定出一种名为 Del-E-222 的病毒,除了在位置 222 处的丙氨酸外,与 Del-E 完全相同。使用 Del-E 骨架的反向遗传学生成了第二种病毒 Del-E-254,其在氨基酸 254 处含有天冬酰胺。测试了 Del-E-222 和 Del-E-254 病毒逃避由肠道外接种提供的中和免疫的能力。用亲本 Del-E 免疫接种并用 Del-E-222 或 Del-E-254 攻毒的鸡的法氏囊中出现了典型的 IBDV 感染的宏观病变,其 B-BW 比值明显小于对照组。显微镜下的病变包括淋巴细胞耗竭,并证实了 Del-E-222 和 Del-E-254 能够突破由亲本 Del-E 病毒接种诱导的免疫力。这两种突变似乎都促成了抗原漂移。