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网状内皮组织增生病病毒长末端重复(LTR)整合入马立克氏病病毒野毒株基因组中功能的评估。

Functional evaluation of the role of reticuloendotheliosis virus long terminal repeat (LTR) integrated into the genome of a field strain of Marek's disease virus.

机构信息

Shandong Agricultural University, Taian 271018, PR China.

出版信息

Virology. 2010 Feb 20;397(2):270-6. doi: 10.1016/j.virol.2009.11.017. Epub 2009 Dec 3.

Abstract

MDV-GX0101 is a field strain of Marek's disease virus with a naturally occurring insertion of the reticuloendotheliosis virus (REV) LTR fragment. In order to study the biological properties of REV-LTR insertion in the MDV genome, we constructed a full-length infectious BAC clone of MDV-GX0101 strain and deleted the LTR sequences by BAC mutagenesis. The pathogenic properties of the LTR-deleted virus were evaluated in infected SPF birds. The study demonstrated that the LTR-deleted virus had a stronger inhibitory effect on the growth rates of the infected birds and induced stronger immunosuppressive effects. Surprisingly, however, the ability for horizontal transmission of the LTR-deleted virus appeared to be significantly weaker than its parental LTR-intact virus. Even though the precise molecular mechanisms are still not clear, the results of our studies demonstrate that the retention of the REV-LTR in the MDV genome decreases its pathogenic effects but increases its potential for horizontal transmission.

摘要

MDV-GX0101 是一株自然携带禽网状内皮组织增生病病毒(REV)LTR 片段插入的马立克氏病病毒野毒株。为了研究 MDV 基因组中 REV-LTR 插入的生物学特性,我们构建了一株全长感染性 BAC 克隆 MDV-GX0101 株,并通过 BAC 诱变缺失 LTR 序列。在感染 SPF 鸡的实验中评估了 LTR 缺失病毒的致病特性。研究表明,LTR 缺失病毒对感染鸡的生长速度具有更强的抑制作用,并诱导更强的免疫抑制作用。然而,令人惊讶的是,LTR 缺失病毒的水平传播能力似乎明显弱于其亲本 LTR 完整病毒。尽管确切的分子机制尚不清楚,但我们的研究结果表明,REV-LTR 在 MDV 基因组中的保留降低了其致病性,但增加了其水平传播的潜力。

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