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中国临床药理学与治疗学 ›› 2002, Vol. 7 ›› Issue (4): 311-313.

• 基础研究 • 上一篇    下一篇

柯萨奇B3 病毒经晚期孕鼠胎盘致母婴感染的小鼠动物模型研究1

盛晓蓉, 吴亦伦, 贾雪梅2, 黄振武3, 吴纳新, 王惠珠2, 齐威琴2, 夏弈明3, 苏诚钦   

  1. 安徽省医学科学研究所病毒室, 合肥 230061;
    2安徽医科大学组织胚胎学教研室, 合肥 230061;
    3中国预防医学科学院营养与食品卫生研究所, 北京 100050
  • 收稿日期:2002-03-27 修回日期:2002-04-18 出版日期:2002-08-26 发布日期:2020-11-24
  • 通讯作者: 盛晓蓉, 女, 副研究员, 主要研究病毒病原学。Tel:0551-2822004 E-mai l:shengxiaorong @ah163. com.
  • 基金资助:
    1 本课题由卫生部科学研究基金( №981066) 资助

Study on experimental model of transplacental infection of coxsackievirus B3 from the mother to the fetus in late gestation mice1

SHENG Xiao-Rong, WU Yi-Lun, JIA Xue-Mei2, HUANG Zhen-Wu3, WU Na-Xin, WANG Hui-Zhu2, QI Wei-Qin2, XIA Yi-Ming3, SU CHENG-Qin   

  1. Department of Virology, Anhui Institute of Medical Sciences, Hefei 230061;
    2Anhui Medical University, Hefei 230061;
    3Chinese Institute of Prevent Medical Sciences, Beijing 100050
  • Received:2002-03-27 Revised:2002-04-18 Online:2002-08-26 Published:2020-11-24

摘要: 目的: 探讨柯萨奇B3 病毒( CVB3m) 在母婴间经胎盘垂直传播的可能性和条件, 并建立小鼠动物模型。方法: 对不同孕期的母鼠分别接种最佳感染量柯萨奇B3 病毒嗜心肌株( CVB3m), 剖腹取胎或产仔。对母鼠、胎鼠、仔鼠及胎盘分别进行病毒学、血清学及病理检查。结果: 晚期孕鼠接种适量的CVB3m后次日形成病毒血症, 此时血中无抗CVB3m中和抗体。病毒经胎盘传播形成母婴垂直感染。胎盘、胎鼠、母鼠心肌及仔鼠血清和心肌中均查到较高滴度的病毒。电镜下可见受染仔鼠心肌细胞线粒体肿胀、嵴突缺失、肌纤维断裂、明暗带模糊等初期病变。结论: 晚期孕鼠感染CVB3m后形成病毒血症, 通过胎盘屏障将病毒传至胎儿, 引起胎鼠及仔鼠心肌病变, 可作为防治CVB3 围产期感染的动物模型。

关键词: 柯萨奇B3病毒, 胎盘传播感染, 病毒血症

Abstract: AIM: To study the possibility and conditions of transplacental infection of coxsackievirus B3(CVB3) from pregnant mice to their fetuses and newborns. METHODS: Coxsackievirus B3 strain causing balb/c mice myocardial injury ( CVB3m ) was inoculated with 105 TCID50 in dose into the mother mice at 6-7 days (early gestation), 9-10 days ( middle gestation) and 17-18 days ( late gestation) of gestation, in contrast with non-pregnant mice. Some placentas and fetuses were removed by caesarean section before mothers partusing; some mothers and their babies were sacrificed after parturition, and virus isolation, serological and pathological tests were performed. RESULTS: Viramiae was observed in mother mice of late-gestation inoculated with CVB3m at a fit amount on the second day after inoculation, while no newtralizing antibody to CVB3m was detected in blood. The virus was isolated from cardiac muscles of inoculated mother mice in different gestation and the controls. The virus was also isolated from some placentas and fetuses, and both sera and cardiac muscles of infants in the late gestation ( virus titer were all 10 -2—10-3). On d 7 of inoculating virus, pregnant and non-pregnant mice titers of neutralizing antibody to CVB3m in sera were all between 1 ∶160 and 1 ∶320. Under the electromicroscopy, some cardiac muscle cells of mother or infant mice appeared with morphological changes and little hollow bubbles occured in cytoplasm. The fibers broke off, and the bright and dark belts became indistinct. CONCLUSION: The amimal model, intraplacental passage of CVB3from pregnant mother in late gestation to fetus in mice, is a benefitial tool to study enterovirus diseases in human perinatal period.

Key words: coxackievirus B3, transplacental infection, viramiae

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