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  1. Home
  2. College of Medicine /醫學院
  3. Institute of Medicine/醫學研究所
  4. 人類博卡病毒殼體蛋白獨立區域對Balb/c小鼠影響之探討
 
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人類博卡病毒殼體蛋白獨立區域對Balb/c小鼠影響之探討

Date Issued
2014
Author(s)
鍾雨涵
Yu-Han Chung
Advisor
徐再靜  
王梅林
URI
https://handle.ncl.edu.tw/11296/gh8zp9
https://scholars.csmu.edu.tw/handle/123456789/36050
Abstract
人類微小病毒B19是微小病毒科中可以感染人類並且致病的病毒。過去研究發現感染B19病毒會造成血管炎、心肌炎、肝炎等疾病。人類博卡病毒HBoV於2005年被發現為可以感染人類並且會引發呼吸道疾病,但是詳細致病機轉仍不清楚。先前實驗室已發現B19-VP1u及HBoV-VP1u皆具有sPLA2活性並可促進發炎細胞激素的表現。並且進一步將B19-VP1u注射至NZB/W F1狼瘡小鼠體內,發現會增加狼瘡小鼠心臟受損,但對於Balb/c小鼠的影響並不清楚。因此本研究利用HBoV-VP1u和B19-VP1u重組蛋白為材料,經由皮下注射方式打入Balb/c小鼠,探討HBoV-VP1u蛋白和B19-VP1u蛋白對小鼠之影響。結果發現B19-VP1u和HBoV-VP1u蛋白會促進Balb/c小鼠肺臟的MMP9活性及蛋白表現。組織病理切片中肺臟細胞也發現有明顯淋巴細胞浸潤的現象。此外,發炎相關蛋白IL-1β及IL-6蛋白表現也明顯增加。由研究結果顯示B19-VP1u蛋白和HBoV-VP1u蛋白會造成呼吸道肺臟損傷。
Human parvovirus B19 (B19) is a pathogenic virus in the family of Parvoviridae. In the past study, it was found that B19 causes disease, such as vasculitis, myocarditis, and hepatitis. From previous studies, it has reported that B19-VP1u contains phospholipase A2 motif and relate with inflammation. Human Bocavirus (HBoV) was found in 2005, it is a pathogenic virus and cause respiratory disease. However, the pathogenesis mechanism is still unclear. In our laboratory studies found that both B19-VP1u and HBoV-VP1u contain sPLA2 activity, they trigger the expression of inflammatory cytokines. Furthermore, we also found that injected B19-VP1u into NZB/W F1 mice cause heart injury. Because it still unclear whether HBoV-VP1u trigger inflammation or not in Balb/c mice. Herein, we want to investigate the influence of HBoV-VP1u and B19-VP1u in Balb/c mice. The results showed that B19-VP1u and HBoV-VP1u increased the activity and protein expression of matrix metalloproteinase (MMP9) in lung. Markedly lymphocyte infiltrations were observed in lungs from Balb/c mice receiving B19-VP1u or HBoV-VP1u. In addition, the inflammatory cytokines IL-1β and IL-6 were significantly increased in lungs from Balb/c mice receiving B19-VP1u or HBoV-VP1u. Theses finding demonstrated that B19-VP1u and HBoV-VP1u trigger inflammation in lung injury.
Type
thesis
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