Rossow K D, Benfield D A, Goyal S M, Nelson E A, Christopher-Hennings J, Collins J E
Department of Veterinary Diagnostic Medicine, University of Minnesota, St. Paul, USA.
Vet Pathol. 1996 Sep;33(5):551-6. doi: 10.1177/030098589603300510.
An immunogold-silver immunohistochemical technique was used to determine the chronological distribution and localization of porcine reproductive and respiratory syndrome virus (PRRSV) in experimentally infected gnotobiotic pigs. Thirty-two pigs were randomly allocated to infected (n = 24) or control (n = 8) groups. Pigs in infected groups were inoculated at 3 days of age by nasal instillation of PRRSV isolate ATCC VR-2332 (total dose = 10(2.64) TCID50), and control pigs were exposed in the same manner to uninfected cell culture supernatant. Three infected and one control pigs were euthanatized at 12 hours and at 1, 2, 3, 5, 7, 14, and 21 days postexposure (DPE). Bronchiolar epithelial cells, arteriolar endothelial cells, monocytes, and interstitial, alveolar, and intravascular macrophages stained for PRRSV antigen at 12 hours postexposure. Staining for PRRSV antigen in endothelial cells, monocytes, and alveolar, interstitial, and intravascular macrophages was most intense and widespread in lung sections from 14 and 21 DPE. In the heart, macrophages in the interstitial and subendocardial spaces and endothelial cells in a few arterioles stained for PRRSV antigen at 14 and 21 DPE. Tonsillar macrophages and mucosal epithelium stained for PRRSV antigen at 12 hours postexposure and sporadically with less intensity in subsequent sampling periods. In the nasal turbinate, PRRSV antigen was identified in macrophages within the mucosal epithelium at 12 hours postexposure and again at 14 and 21 DPE. There was focal staining for PRRSV antigen in the choroid plexus in one pig at 14 DPE. Based on the results of this experiment, the pathogenesis of PRRSV infection in gnotobiotic pigs can be described as initial virus entry through nasal epithelial, tonsillar, and pulmonary macrophages, with viremia occurring by 12 hours postexposure followed by the development of pneumonia, myocarditis, encephalitis, rhinitis, vasculitis, and lymphoid necrosis. Although PRRSV can infect macrophages in heart, tonsil, turbinate, and choroid plexus, pulmonary macrophages are predominantly and consistently infected and are the predominantly cells for virus replication in gnotobiotic pigs.
采用免疫金银免疫组织化学技术，确定猪繁殖与呼吸综合征病毒（PRRSV）在实验感染的无菌猪体内的时间分布和定位。32头猪被随机分为感染组（n = 24）和对照组（n = 8）。感染组的猪在3日龄时通过滴鼻接种PRRSV分离株ATCC VR - 2332（总剂量 = 10(2.64) TCID50），对照组猪以相同方式暴露于未感染的细胞培养上清液。在暴露后12小时以及暴露后1、2、3、5、7、14和21天，对3头感染猪和1头对照猪实施安乐死。暴露后12小时，细支气管上皮细胞、小动脉内皮细胞、单核细胞以及间质、肺泡和血管内巨噬细胞出现PRRSV抗原染色。在暴露后14天和21天的肺切片中，内皮细胞、单核细胞以及肺泡、间质和血管内巨噬细胞中的PRRSV抗原染色最为强烈且广泛。在心脏中，间质和心内膜下间隙的巨噬细胞以及少数小动脉中的内皮细胞在暴露后14天和21天出现PRRSV抗原染色。扁桃体巨噬细胞和黏膜上皮在暴露后12小时出现PRRSV抗原染色，在随后的采样期偶尔出现且强度较低。在鼻甲骨中，黏膜上皮内的巨噬细胞在暴露后12小时以及暴露后14天和21天再次出现PRRSV抗原。在1头猪的脉络丛中，暴露后14天出现PRRSV抗原的局灶性染色。基于该实验结果，无菌猪PRRSV感染的发病机制可描述为病毒最初通过鼻上皮、扁桃体和肺巨噬细胞进入，暴露后12小时出现病毒血症，随后发展为肺炎、心肌炎、脑炎、鼻炎、血管炎和淋巴组织坏死。虽然PRRSV可感染心脏、扁桃体、鼻甲骨和脉络丛中的巨噬细胞，但肺巨噬细胞是主要且持续被感染的细胞，是无菌猪体内病毒复制的主要细胞。
