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导致传染性法氏囊病双 RNA 病毒(IBDV)抗原漂移的氨基酸。

Amino acids contributing to antigenic drift in the infectious bursal disease Birnavirus (IBDV).

机构信息

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.

出版信息

Virology. 2011 Jan 5;409(1):33-7. doi: 10.1016/j.virol.2010.09.030. Epub 2010 Oct 20.

Abstract

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.

摘要

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。

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