马立克病神经病变的发病机制。2来自患病供体的脾脏细胞传递神经病变[作者译]。

G Hoffmann-Fezer, W Schmahl, R Hoffmann
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引用次数: 0

摘要

将13只有马立克病临床和组织学表现的鸡的活脾淋巴细胞静脉注射到46只4-10日龄的鸡身上,接种前24小时x线检查。6-14 d后,组织学上几乎有规律地观察到马立克样神经病变。接受马立克供体破坏的脾脏淋巴细胞的鸡无神经浸润。在单独应用致病性马立克氏病病毒或与来自免疫马立克氏病的健康供体的活脾细胞联合使用后14天内,也没有检测到神经损伤。这些结果排除了脾脏细胞移植后6-14天神经病变的形成完全是由病毒引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Pathogenesis of neural lesions in Marek's disease. II. Transmission of neural lesions by spleen cells from ill donors (author's transl) ].

Viable spleen lymphocytes of 13 chickens with clinical and histological signs of Marek's disease were transferred by intravenous injection to 46 chickens 4-10 days old, X-rayed 24 hours before inoculation. Histologically Marek-like neural lesions were almost regularly observed in the chickens after 6-14 days. Chickens having received destroyed spleen lymphocytes of Marek-donors were free of nerve infiltrations. There were also no neural lesions detectable within 14 days after application of pathogenic Marek's disease virus alone, or in combination with viable spleen cells from healthy donors immunized against Marek's disease. These results exclude that the formation of neural lesions 6-14 days following the spleen cell transfer is solely induced by the virus.

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