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本文引用的文献

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The pathogenicity determinant of Citrus tristeza virus causing the seedling yellows syndrome maps at the 3'-terminal region of the viral genome.导致柑橘衰退病毒种苗黄化综合征的病原决定因子定位于病毒基因组的 3'-末端区。
Mol Plant Pathol. 2010 Jan;11(1):55-67. doi: 10.1111/j.1364-3703.2009.00572.x.
2
Tandem leader proteases of Grapevine leafroll-associated virus-2: host-specific functions in the infection cycle.葡萄卷叶相关病毒2的串联前导蛋白酶:感染周期中的宿主特异性功能
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Molecular variability of the 5'- and 3'-terminal regions of citrus tristeza virus RNA.柑橘衰退病毒 RNA 5'-和 3'-末端区的分子变异性。
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Genetic Marker Analysis of a Global Collection of Isolates of Citrus tristeza virus: Characterization and Distribution of CTV Genotypes and Association with Symptoms.柑橘碎叶病毒全球分离物的遗传标记分析:CTV 基因型的特征和分布及其与症状的关系。
Phytopathology. 2005 Aug;95(8):909-17. doi: 10.1094/PHYTO-95-0909.
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The specific involvement of coat protein in tobacco mosaic virus cross protection.外壳蛋白在烟草花叶病毒交叉保护中的具体作用。
Virology. 1982 May;119(1):150-8. doi: 10.1016/0042-6822(82)90072-1.
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A similarity between viral defense and gene silencing in plants.植物中病毒防御与基因沉默之间的相似性。
Science. 1997 Jun 6;276(5318):1558-60. doi: 10.1126/science.276.5318.1558.
7
Three genes of Citrus tristeza virus are dispensable for infection and movement throughout some varieties of citrus trees.柑橘衰退病毒的三个基因对于在某些柑橘树品种中的感染和传播并非必需。
Virology. 2008 Jul 5;376(2):297-307. doi: 10.1016/j.virol.2007.12.038. Epub 2008 May 5.
8
Citrus tristeza virus: survival at the edge of the movement continuum.柑橘衰退病毒:在移动连续体边缘的存活
J Virol. 2008 Jul;82(13):6546-56. doi: 10.1128/JVI.00515-08. Epub 2008 Apr 23.
9
Persistent infection and promiscuous recombination of multiple genotypes of an RNA virus within a single host generate extensive diversity.在单个宿主中,一种 RNA 病毒的持续感染和多种基因型的混杂重组会产生广泛的多样性。
PLoS One. 2007 Sep 19;2(9):e917. doi: 10.1371/journal.pone.0000917.
10
Semliki Forest virus vectors with mutations in the nonstructural protein 2 gene permit extended superinfection of neuronal and non-neuronal cells.在非结构蛋白2基因中发生突变的辛德毕斯病毒载体可使神经元细胞和非神经元细胞的重复感染时间延长。
J Neurovirol. 2007 Aug;13(4):353-63. doi: 10.1080/13550280701393204.

感染甜橙衰退病毒的株系并不排除被其他株系的病毒再次感染。

Infection with strains of Citrus tristeza virus does not exclude superinfection by other strains of the virus.

机构信息

Citrus Research and Education Center, University of Florida, 700 Experiment Station Road, Lake Alfred, Florida 33850, USA.

出版信息

J Virol. 2010 Feb;84(3):1314-25. doi: 10.1128/JVI.02075-09. Epub 2009 Nov 18.

DOI:10.1128/JVI.02075-09
PMID:19923189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2812332/
Abstract

Superinfection exclusion or homologous interference, a phenomenon in which a primary viral infection prevents a secondary infection with the same or closely related virus, has been observed commonly for viruses in various systems, including viruses of bacteria, plants, and animals. With plant viruses, homologous interference initially was used as a test of virus relatedness to define whether two virus isolates were "strains" of the same virus or represented different viruses, and subsequently purposeful infection with a mild isolate was implemented as a protective measure against isolates of the virus causing severe disease. In this study we examined superinfection exclusion of Citrus tristeza virus (CTV), a positive-sense RNA closterovirus. Thirteen naturally occurring isolates of CTV representing five different virus strains and a set of isolates originated from virus constructs engineered based on an infectious cDNA clone of T36 isolate of CTV, including hybrids containing sequences from different isolates, were examined for their ability to prevent superinfection by another isolate of the virus. We show that superinfection exclusion occurred only between isolates of the same strain and not between isolates of different strains. When isolates of the same strain were used for sequential plant inoculation, the primary infection provided complete exclusion of the challenge isolate, whereas isolates from heterologous strains appeared to have no effect on replication, movement or systemic infection by the challenge virus. Surprisingly, substitution of extended cognate sequences from isolates of the T68 or T30 strains into T36 did not confer the ability of resulting hybrid viruses to exclude superinfection by those donor strains. Overall, these results do not appear to be explained by mechanisms proposed previously for other viruses. Moreover, these observations bring an understanding of some previously unexplained fundamental features of CTV biology and, most importantly, build a foundation for the strategy of selecting mild isolates that would efficiently exclude severe virus isolates as a practical means to control CTV diseases.

摘要

超感染排除或同源干扰,即一种主要的病毒感染阻止了同一种或密切相关的病毒的二次感染,这种现象在各种系统的病毒中都很常见,包括细菌、植物和动物的病毒。在植物病毒中,同源干扰最初被用作病毒相关性的测试,以确定两个病毒分离物是否为同一病毒的“株”,还是代表不同的病毒,随后有目的地用温和的分离物进行感染,作为预防引起严重疾病的病毒分离物的保护措施。在这项研究中,我们研究了柑橘衰退病毒(CTV)的超感染排除现象,CTV 是一种正链 RNA 闭合病毒。我们研究了 13 种自然发生的 CTV 分离物,代表了五个不同的病毒株系和一组源自基于 CTV T36 分离物的传染性 cDNA 克隆的分离物,包括含有不同分离物序列的杂种,以研究它们防止另一种病毒分离物超感染的能力。我们表明,超感染排除仅发生在同一株系的分离物之间,而不是不同株系的分离物之间。当同一株系的分离物用于连续植物接种时,原发性感染完全排除了挑战分离物,而来自异源株系的分离物似乎对挑战病毒的复制、运动或系统感染没有影响。令人惊讶的是,将 T68 或 T30 株系的扩展同源序列取代到 T36 中并没有赋予这些杂种病毒排除供体株系超感染的能力。总的来说,这些结果似乎不能用以前提出的其他病毒的机制来解释。此外,这些观察结果使我们对 CTV 生物学的一些以前未解释的基本特征有了更深入的了解,最重要的是,为选择温和分离物的策略奠定了基础,该策略可以有效地排除严重的病毒分离物,作为控制 CTV 疾病的一种实用手段。