Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/63313
標題: Effect of the Loop Regions of Infectious Bursal Disease Virus on Receptor Binding and Viral Pathology
傳染性華氏囊炎病毒表面凸出區域與受體結合及影響致病力之研究
作者: 王敏盈
賴素媛
林全信
關鍵字: 生物技術
商品化
infectious bursal disease virus
subviral particle
attachment
immobilized metal-ion affinity chromatography
receptor
摘要: Infectious bursal disease virus (IBDV) causes a highly contagious disease in young chicksand leads to significant economic losses in the poultry industry. The capsid protein VP2 ofIBDV plays an important role in virus binding and cell recognition. VP2 forms a subviralparticle (SVP) with a similar immunogenicity as the IBDV capsid. Previously, we showed thatSVP could dose-dependently inhibit IBDV infection to an IBDV susceptible cell line, DF-1cells. Furthermore, the SVP attachment to DF-1 cells was inhibited by an SVP-inducedneutralizing monoclonal antibody against IBDV but not by denatured-VP2-inducedpolyclonal antibodies. Then, the cellular factors in DF-1 cells involving in the attachment ofSVP were purified by affinity chromatography using SVP bound on the immobilized Ni+2 ions.A dominant factor was identified as chicken heat shock protein 90 (cHsp90) by massspectrometry and for the first time, our results suggest that cHsp90 is part of the putativecellular receptor complex essential for IBDV entry to DF-1 cells. A three-year project isproposed to fully understand the role of VP2 protrusion domain involved in IBDV entry andin IBDV pathology. Three specific aims will be finished. The first is to study the entry ofIBDV and subviral particles into cells using various physical and chemical techniques, then tounderstand the role of VP2 protrusion domain involved in the entry of SVP by site-directedmutagenesis and finally to understand the role of VP2 protrusion domain involved in thepathology of IBDV by reverse genetics approach. Understanding the IBDV entry willfacilitate the development of an alternative way to prevent the IBDV infection.
傳染性華氏囊炎病毒(IBDV)對於幼雞隻具有高度傳染性,受感染的幼雞其免疫功能遭破壞,導致死亡率上升,因而造成養雞業者經濟上的重大損失。據先前研究之結果推測IBDV 的外鞘( capsid )蛋白VP2 參與病毒接受體的結合,且具有辨識宿主細胞的功能。當利用昆蟲細胞表現系統單獨表現VP2 蛋白時,VP2 會自我組裝成一粒徑大小為25 nm 的次病毒顆粒( 簡稱為VP2 SVP )。對於病毒宿主細胞DF-1 (分離自雞胚纖維母細胞之細胞株)而言,VP2 SVP 具有抑制其遭受病毒感染的效果,利用VP2 SVP 取代真實病毒顆粒並結合至固定化Ni+2 金屬離子親和性管柱( IMAC )上已分離出雞Heat shockprotein 90 ( chicken Hsp90 )為IBDV 病毒的受體複合體之一分子。為更了解IBDV 進入細胞之機制,後續如何開啟病毒複製與致病之過程以便開發抑制病毒感染的新方法,本計劃將分三年三階段針對傳染性華氏囊炎病毒表面凸出(protrusion)區域與受體結合的情形及其如何影響致病力作進一步之探討,這三階段的目標分別為:1. 探討IBDV 與次病毒顆粒停留與進入細胞膜的情形;2. 探討次病毒顆粒表面凸出(protrusion)區域如何影響次病毒顆粒停留與進入細胞膜;3. 探討IBDV 病毒表面凸出(protrusion)區域如何影響病毒感染細胞之能力及致病力。
URI: http://hdl.handle.net/11455/63313
其他識別: NSC100-2321-B005-004-MY3
文章連結: http://grbsearch.stpi.narl.org.tw/GRB/result.jsp?id=2348089&plan_no=NSC100-2321-B005-004-MY3&plan_year=100&projkey=PD10007-0311&target=plan&highStr=*&check=0&pnchDesc=%E5%82%B3%E6%9F%93%E6%80%A7%E8%8F%AF%E6%B0%8F%E5%9B%8A%E7%82%8E%E7%97%85%E6%AF%92%E8%A1%A8%E9%9D%A2%E5%87%B8%E5%87%BA%E5%8D%80%E5%9F%9F%E8%88%87%E5%8F%97%E9%AB%94%E7%B5%90%E5%90%88%E5%8F%8A%E5%BD%B1%E9%9F%BF%E8%87%B4%E7%97%85%E5%8A%9B%E4%B9%8B%E7%A0%94%E7%A9%B6
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