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表达传染性法氏囊病病毒VP2的禽腺病毒重组体诱导针对法氏囊病的保护性免疫。

Fowl adenovirus recombinant expressing VP2 of infectious bursal disease virus induces protective immunity against bursal disease.

作者信息

Sheppard M, Werner W, Tsatas E, McCoy R, Prowse S, Johnson M

机构信息

CSIRO, Division of Animal Health, Animal Health Research Laboratory, Victoria, Australia.

出版信息

Arch Virol. 1998;143(5):915-30. doi: 10.1007/s007050050342.

DOI:10.1007/s007050050342
PMID:9645198
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7087160/
Abstract

The right hand end Nde I fragment 3 (90.8-100 map units) of the fowl adenovirus serotype 10 (FAV-10) was characterised so as to allow the location of an insertion site for recombinant vector construction. Infectious bursal disease virus (IBDV) VP2 gene from the Australian classical strain 002/73, under the control of the FAV-10 major late promoter/leader sequence (MLP/LS) was inserted into a unique Not I site that was generated at 99.5 map units. This recombinant virus was produced without deletion of any portion of the FAV-10 genome. When administered to specific pathogen free (SPF) chickens intravenously, intraperitoneally, subcutaneously or intramuscularly, it was shown that the FAV-10/VP2 recombinant induced a serum VP2 antibody response and protected chickens against challenge with IBDV V877, an intermediate virulent classical strain. Birds were not protected when the recombinant was delivered via the conjunctival sac.

摘要

对禽腺病毒10型(FAV - 10)右手端Nde I片段3(90.8 - 100图谱单位)进行了特征分析,以便确定重组载体构建的插入位点。来自澳大利亚经典毒株002/73的传染性法氏囊病病毒(IBDV)VP2基因,在FAV - 10主要晚期启动子/前导序列(MLP/LS)的控制下,被插入到在99.5图谱单位处产生的一个独特的Not I位点。该重组病毒的产生未导致FAV - 10基因组的任何部分缺失。当通过静脉内、腹腔内、皮下或肌肉内途径给无特定病原体(SPF)鸡接种时,结果表明FAV - 10/VP2重组体诱导了血清VP2抗体反应,并保护鸡免受中间毒力经典毒株IBDV V877的攻击。当通过结膜囊接种该重组体时,鸡未受到保护。

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