Viral replication and lesions in BALB/c mice experimentally inoculated with porcine circovirus isolated from a pig with postweaning multisystemic wasting disease

Viral replication and lesions in BALB/c mice experimentally inoculated with porcine circovirus isolated from a pig with postweaning multisystemic wasting disease
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DOI:
10.1354/vp.38-1-74
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发表时间:
2001-01-01
影响因子:
2.4
通讯作者:
Mittal, SK
Mittal, SK
中科院分区:
农林科学2区
文献类型:
--
作者:
Kiupel, M;Stevenson, GW;Mittal, SK

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对8周龄BALB/c小鼠进行假接种(对照小鼠)或腹腔内(IP)和鼻内(IN)接种单剂量(sPCV小鼠)或多剂量(mPCV小鼠)猪圆环病毒2型(PCV 2)。接种后7、14、28和42天(PI)处死4只对照小鼠和4只sPCV小鼠。PI 42天处死所有4只mPCV小鼠。此外,对妊娠7天和14天的BALB/c小鼠进行假接种(对照小鼠)或IP和LN接种单剂量PCV 2。在出生后1、8和15天对新生小鼠实施安乐死。对所有安乐死小鼠进行尸检,并收集组织进行组织病理学、电子显微镜、原位杂交和聚合酶链反应(PCR)。PCV 2在接种PCV 2的8周龄BALB/c小鼠中复制,并在妊娠7天和14天接种妊娠BALB/c小鼠时引起胎儿感染。通过原位杂交和PCR在感染后第7、14、28和42天的sPCV小鼠中检测到PCV;在感染后第42天的mPCV小鼠中检测到PCV;在出生后第1、8和15天的妊娠7天和14天接种PCV的母亲的新生小鼠中检测到PCV,但对照小鼠中未检测到PCV。研究期间,在sPCV或mPCV小鼠中未发现临床体征或肉眼病变。sPCV小鼠和mPCV小鼠的显微镜病变特征为淋巴器官中的生发中心扩张,具有大量组织细胞和淋巴母细胞,生发中心中的组织细胞凋亡,以及副皮质的轻度淋巴耗竭。PCV核酸在淋巴组织生发中心的组织细胞和凋亡细胞的细胞核和细胞质中以及在肝脏的肝细胞核中、在肾小管上皮细胞的细胞核中和在胸腺的单个淋巴细胞的细胞质中检测到。先天性感染小鼠仅在肝脏中推定的枯否细胞中检测到PCV核酸。
Eight-week-old BALB/c mice were either sham inoculated (control mice) or were inoculated intraperitoneally (IP) and intranasally (IN) with a single (sPCV mice) or multiple (mPCV mice) doses of porcine circovirus 2 (PCV2). Four control mice and 4 sPCV mice were sacrificed 7, 14, 28, and 42 days postinoculation (PI). All 4 mPCV mice were sacrificed 42 days PI. In addition, 7-day and 14-day pregnant BALB/c mice were either sham inoculated (control mice) or were inoculated IP and LN with a single dose of PCV2. Newborn mice were euthanatized 1, 8, and 15 days after birth. Necropsies were performed on all euthanatized mice and tissues were collected for histopathology, electron microscopy, in situ hybridization, and polymerase chain reaction (PCR). PCV2 replicated in 8-week-old BALB/c mice that were inoculated with PCV2 and caused fetal infection when inoculated into pregnant BALB/c mice at 7 days and 14 days of gestation. PCV was detected by in situ hybridization and PCR in sPCV mice on days 7, 14, 28, and 42 PI; in mPCV mice on day 42 PI; and in newborn mice from mothers inoculated with PCV at 7 days and 14 days of gestation at 1, 8, and 15 days after birth, but not in control mice. No clinical signs or gross lesions were found in sPCV or mPCV mice during the study. Microscopic lesions in sPCV mice and mPCV mice were characterized by expansion of germinal centers in lymphoid organs with large numbers of histiocytic cells and lymphoblasts, apoptosis of histiocytic cells in germinal centers, and mild lymphoid depletion of the paracortex. PCV nucleic acid was detected in the nuclei and cytoplasm of histiocytes and apoptotic cells in germinal centers in lymphoid tissues as well as in the nuclei of hepatocytes in the liver, in the nuclei of renal tubular epithelial cells, and in the cytoplasm of single lymphocytes in the thymus. Congenitally infected mice only had PCV nucleic acid detected in putative Kupffer cells in livers.