The M, F and HN genes of genotype VIId Newcastle disease virus are associated with the severe pathological changes in the spleen of chickens.

The M, F and HN genes of genotype VIId Newcastle disease virus are associated with the severe pathological changes in the spleen of chickens.
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VIId基因型新城疫病毒的M、F和HN基因与鸡脾脏的严重病理改变有关。

DOI:
10.1186/s12985-015-0366-5
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发表时间:
2015-09-04
期刊:
影响因子:
4.8
通讯作者:
Liu X
Liu X
中科院分区:
医学3区
文献类型:
--
作者:
Kai Y;Hu Z;Xu H;Hu S;Zhu J;Hu J;Wang X;Liu X;Liu X

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与其他强毒株相比,基因型 VIId 新城疫病毒 (NDV) 株可引起更严重的淋巴器官组织损伤。人们对潜在的分子机制知之甚少。基因型 IV NDV Herts/33 和基因型 VIId NDV JS5/05 在脾脏中具有独特的病理特征。选择这两株病毒作为亲本病毒,通过反向遗传单独替换Herts/33的M、F和HN基因或与JS5/05的相应基因组合,产生一组嵌合病毒。评估了重组病毒的毒力和体外特征。此外,还分析了感染这些重组病毒的鸡脾脏的病理变化、病毒载量和转录细胞因子反应。致病性测试表明,所有嵌合病毒均具有毒力。体外表征表明,基因替换不会改变重组病毒的生长动力学和细胞表面的 HN 表达。然而,M、F 和 HN 基因的替换导致融合活性发生明显变化。此外,病理学研究表明,仅在Herts/33骨干中包含JS5/05的同源M、F和HN基因会导致严重的病理变化,其特征是脾脏广泛坏死,与JS5/05引起的情况类似。此外,与 Herts/33 相比,这种基因替换显着增加了病毒复制和转录细胞因子反应水平。相反,与JS5/05相比,将Herts/33的M、F和HN基因纳入JS5/05主链会导致Herts/33特异性病理变化,并显着降低病毒载量和细胞因子基因的表达水平。 M、F和HN基因与感染VIId基因型NDV鸡的脾脏严重病变有关。
The strains of the genotype VIId Newcastle disease virus (NDV) induce more severe tissue damage in lymphoid organs than other virulent strains. The underlying molecular mechanisms are poorly understood. Genotype IV NDV Herts/33 and genotype VIId NDV JS5/05 have a distinctive pathological profile in the spleen. These two strains of viruses were selected as parental viruses to generate a panel of chimeric viruses by replacing the M, F and HN genes of Herts/33 individually or in combination with the corresponding genes of JS5/05 using reverse genetic. Virulence and in vitro characteristics of the recombinant viruses were assessed. In addition, pathological changes, virus load, and transcriptional cytokine response in the spleen of chickens infected with these recombinant viruses were also analyzed. Pathogenicity test showed that all chimeric viruses are virulent. In vitro characterization revealed that gene replacement did not change growth kinetics and HN expression on cell surface of the recombinant viruses. However, replacement of the M, F and HN genes resulted in apparent changes in the fusion activity. Moreover, pathological studies revealed that only inclusion of the homologous M, F and HN genes of JS5/05 in Herts/33 backbone resulted in severe pathological changes characterized by extensive necrosis in the spleen, similar to that induced by JS5/05. In addition, this gene replacement significantly increased virus replication and the levels of transcriptional cytokine response, compared to Herts/33. Conversely, inclusion of the M, F and HN genes of Herts/33 into JS5/05 backbone resulted in Herts/33-specific pathological changes and significantly decreased virus load and the expression levels of cytokine genes, compared to JS5/05. The M, F and HN genes are related to the severe pathological changes in the spleen of chickens infected with genotype VIId NDV.