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高致病性猪繁殖与呼吸综合征病毒在猪群中的致病性与分布。

Pathogenicity and distribution of highly pathogenic porcine reproductive and respiratory syndrome virus in pigs.

机构信息

State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China.

出版信息

Transbound Emerg Dis. 2013 Aug;60(4):351-9. doi: 10.1111/j.1865-1682.2012.01354.x. Epub 2012 Jul 5.

DOI:10.1111/j.1865-1682.2012.01354.x
PMID:22762447
Abstract

The pathogenesis of highly pathogenic porcine reproductive and respiratory syndrome virus (PRRSV) strain (HuN4) is poorly understood. Therefore, highly pathogenic PRRSV strain (HuN4) and its derivative strain (HuN4-F112) (obtained by propagation in MARC145 cells for 112 passages) were inoculated into a total of 48 PRRSV-sero-negative pigs (age: 4-5 weeks) by the intranasal route. Virological, pathological and in situ hybridization analyses were performed. The results exhibited that pigs infected with HuN4 showed a loss of appetite, decrease in body weight, raised body temperature and respiratory symptoms, along with interstitial pneumonia lesions. In the HuN4 group, multifocal interstitial pneumonia with macrophage infiltration was found in the lung. The lesions in the lymph node were characterized by collapsed follicles, depletion of germinal centres and reduction in lymphocytes. Perivascular cuffing and glial nodules were observed in the brains of some pigs. By comparison, the HuN4-F112 group had milder lesions. PRRSV was detected in macrophages, alveolar epithelial cells and vascular endothelial cells in the tonsil and lymph nodes. The PRRSV amounts in the pigs infected with HuN4 were 10(5) -10(9) copies/ml in the blood and 10(10) -10(11) copies/g in the lung tissues, whereas the virus amounts with HuN4-F112 were 10(2.15) -10(3.13) copies/ml in the blood and 10(3.0) -10(3.6) copies/g in the lung. Our results demonstrate that the PRRS HuN4 virus infects alveolar epithelial cells, macrophages and vascular endothelial cells causing diffuse alveolar damage and lymph node necrosis. Its higher pathogenicity compared with HuN4-F112 virus may be explained in part by higher replication rate in the previously mentioned organs.

摘要

高致病性猪繁殖与呼吸综合征病毒(PRRSV)毒株(HuN4)的发病机制尚不清楚。因此,我们通过鼻腔途径将高致病性 PRRSV 毒株(HuN4)及其衍生毒株(HuN4-F112)(在 MARC145 细胞中传代 112 代获得)接种到 48 头 PRRSV 血清阴性猪(年龄:4-5 周)中。进行了病毒学、病理学和原位杂交分析。结果表明,感染 HuN4 的猪表现出食欲不振、体重减轻、体温升高和呼吸症状,同时伴有间质性肺炎病变。在 HuN4 组中,肺部发现多灶性间质性肺炎伴巨噬细胞浸润。淋巴结病变的特征是滤泡塌陷、生发中心耗竭和淋巴细胞减少。一些猪的脑中有血管周围套袖和神经胶质结节。相比之下,HuN4-F112 组的病变较轻。在扁桃体和淋巴结的巨噬细胞、肺泡上皮细胞和血管内皮细胞中检测到 PRRSV。感染 HuN4 的猪血液中的 PRRSV 量为 10(5)-10(9)拷贝/ml,肺组织中的病毒量为 10(10)-10(11)拷贝/g,而 HuN4-F112 的病毒量为 10(2.15)-10(3.13)拷贝/ml,肺组织中的病毒量为 10(3.0)-10(3.6)拷贝/g。我们的结果表明,PRRS HuN4 病毒感染肺泡上皮细胞、巨噬细胞和血管内皮细胞,导致弥漫性肺泡损伤和淋巴结坏死。与 HuN4-F112 病毒相比,其更高的致病性可能部分解释为在上述器官中更高的复制率。

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