• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

[通过用鸭乙型肝炎病毒蛋白免疫鸭乙型肝炎病毒携带鸭引发肝炎的尝试]

[Attempt to cause hepatitis in duck hepatitis B virus carrier ducks by immunization with DHBV protein].

作者信息

Kohge N, Fukuda R

机构信息

Second Department of Internal Medicine, Shimane Medical University, Izumo, Japan.

出版信息

Nihon Shokakibyo Gakkai Zasshi. 1992 May;89(5):1242-51.

PMID:1619786
Abstract

In order to investigate the hypothesis that viral hepatitis is a host immune response against viral protein presented on hepatocytes, we attempted to cause hepatitis in DHBV carrier ducks by immunization with DHBV protein. While ducks injected with Freund Complete Adjuvant (FCA) showed only weak hepatitis, those immunized with DHBV particle protein showed severe hepatitis. This same procedure could not cause significant inflammation in the liver of ducks without DHBV infection. The severity of hepatitis was well associated with the frequency of the immunization. However, the degree of hepatitis activity was different among same times immunized ducks. Occurrence of hepatitis assumed to have close association with host immune response against viral protein.

摘要

为了研究病毒性肝炎是宿主针对肝细胞上呈现的病毒蛋白的免疫反应这一假说,我们尝试通过用鸭乙肝病毒(DHBV)蛋白免疫DHBV携带鸭来引发肝炎。虽然注射弗氏完全佐剂(FCA)的鸭仅表现出轻微肝炎,但用DHBV颗粒蛋白免疫的鸭则表现出严重肝炎。相同的程序在未感染DHBV的鸭肝脏中不会引起明显炎症。肝炎的严重程度与免疫频率密切相关。然而,在相同时间免疫的鸭中,肝炎活动程度有所不同。肝炎的发生被认为与宿主针对病毒蛋白的免疫反应密切相关。

相似文献

1
[Attempt to cause hepatitis in duck hepatitis B virus carrier ducks by immunization with DHBV protein].[通过用鸭乙型肝炎病毒蛋白免疫鸭乙型肝炎病毒携带鸭引发肝炎的尝试]
Nihon Shokakibyo Gakkai Zasshi. 1992 May;89(5):1242-51.
2
Inflammation of the liver causes mutations in duck hepatitis B virus genome.肝脏炎症会导致鸭乙型肝炎病毒基因组发生突变。
Gastroenterol Jpn. 1993 Apr;28(2):254-8. doi: 10.1007/BF02779228.
3
Antiviral therapy with entecavir combined with post-exposure "prime-boost" vaccination eliminates duck hepatitis B virus-infected hepatocytes and prevents the development of persistent infection.恩替卡韦抗病毒治疗联合暴露后“初免-加强”疫苗接种可清除鸭乙型肝炎病毒感染的肝细胞,并预防持续性感染的发生。
Virology. 2008 Apr 10;373(2):329-41. doi: 10.1016/j.virol.2007.11.032. Epub 2008 Jan 18.
4
Epitope-specific antibody response to the surface antigen of duck hepatitis B virus in infected ducks.感染鸭体内针对鸭乙型肝炎病毒表面抗原的表位特异性抗体反应。
Virology. 1990 Jun;176(2):546-52. doi: 10.1016/0042-6822(90)90025-m.
5
Vaccination of ducks with a whole-cell vaccine expressing duck hepatitis B virus core antigen elicits antiviral immune responses that enable rapid resolution of de novo infection.用表达鸭乙型肝炎病毒核心抗原的全细胞疫苗对鸭子进行接种可引发抗病毒免疫反应,从而能够迅速消除新出现的感染。
Virology. 2006 May 10;348(2):297-308. doi: 10.1016/j.virol.2005.12.032. Epub 2006 Feb 8.
6
Elimination of immune tolerance to hepatitis virus in an animal model.在动物模型中消除对肝炎病毒的免疫耐受。
Chin Med J (Engl). 1992 Mar;105(3):199-203.
7
Covalently closed circular DNA is the predominant form of duck hepatitis B virus DNA that persists following transient infection.共价闭合环状DNA是鸭乙型肝炎病毒DNA的主要形式,在短暂感染后持续存在。
J Virol. 2005 Oct;79(19):12242-52. doi: 10.1128/JVI.79.19.12242-12252.2005.
8
IFN-gamma increases efficiency of DNA vaccine in protecting ducks against infection.干扰素-γ提高DNA疫苗保护鸭免受感染的效率。
World J Gastroenterol. 2005 Aug 28;11(32):4967-73. doi: 10.3748/wjg.v11.i32.4967.
9
Duck hepatitis B virus infection and duck hepatocellular carcinoma.鸭乙型肝炎病毒感染与鸭肝细胞癌
Chin Med J (Engl). 1992 Mar;105(3):217-26.
10
Contribution of aflatoxin B1 and hepatitis B virus infection in the induction of liver tumors in ducks.黄曲霉毒素B1和乙型肝炎病毒感染在鸭肝脏肿瘤诱导中的作用。
Cancer Res. 1990 Apr 1;50(7):2156-63.

引用本文的文献

1
Inflammation of the liver causes mutations in duck hepatitis B virus genome.肝脏炎症会导致鸭乙型肝炎病毒基因组发生突变。
Gastroenterol Jpn. 1993 Apr;28(2):254-8. doi: 10.1007/BF02779228.