A VP24-truncated isolate of white spot syndrome virus is inefficient in per os infection.

A VP24-truncated isolate of white spot syndrome virus is inefficient in per os infection.
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VP24 截短的白斑综合症病毒分离株在经口感染中效率低下

DOI:
10.1186/s13567-017-0492-8
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发表时间:
2017-12-11
影响因子:
4.4
通讯作者:
Yang F
Yang F
中科院分区:
农林科学2区
文献类型:
--
作者:
Han Y;Li F;Xu L;Yang F

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白色斑点综合征病毒(WSSV)是对虾的主要病原。在此,我们从自然感染的对虾中鉴定了一个新的WSSV毒株,WSSV-CN 04。全基因组测序结果表明,WSSV-CN 04基因组全长281 054 bp,编码157个蛋白。WSSV-CN 04株基因组序列与弱毒株WSSV-CN 03株基因组序列同源性最高,为97.5%。值得注意的是,在WSSV-CN 04中,主要包膜蛋白VP 24不仅被截短,而且在病毒粒子中缺失。由于VP 24介导WSSV与几丁质的相互作用,是WSSV经口感染凡纳滨对虾所必需的,因此我们进一步分析了WSSV-CN 03和-CN 04经口感染凡纳滨对虾的情况,发现WSSV-CN 04的感染力显著低于WSSV-CN 03。与感染WSSV-CN 03的对虾相比,感染WSSV-CN 04的对虾在感染后4小时(hpi)在消化道组织中检测到较少的病毒粒子,并且在24 hpi动物中的病毒滴度低得多。此外,对应于VP 24几丁质结合结构域的肽将中肠中WSSV-CN 03的量减少到与4 hpi时WSSV-CN 04的量相似的水平。这些结果表明,VP 24的截短可能会减弱WSSV-CN 04的经口感染性,从而验证了VP 24在WSSV经口感染中的重要作用。本文的在线版本(10.1186/s13567-017-0492-8)包含补充材料,可供授权用户使用。
White spot syndrome virus (WSSV) is a major pathogen of penaeid shrimp. Here we identified a new WSSV strain, WSSV-CN04, from naturally infected Marsupenaeus japonicus. Whole genomic sequencing results indicate that the WSSV-CN04 genome was 281 054 bp in length, and encoded 157 hypothetic proteins. The genome sequence of WSSV-CN04 was most closely related to the low-virulent strain WSSV-CN03, sharing 97.5% sequence identity. Notably, in WSSV-CN04, the major envelop protein VP24 was not only truncated but also absent in the virions. Since VP24 was previously reported to be essential for WSSV per os infection by mediating WSSV-chitin interaction, we further analyzed the peroral infection of WSSV-CN03 and -CN04 in Litopenaeus vannamei, and show that the infectivity of WSSV-CN04 was significantly lower than that of WSSV-CN03. When compared with WSSV-CN03-infected shrimp, fewer virions were detected in the digestive tract tissues of WSSV-CN04-infected shrimp at 4 hours post-infection (hpi), and the viral titers in the animals at 24 hpi were much lower. Moreover, a peptide corresponding to VP24 chitin-binding domain reduced the amount of WSSV-CN03 in the midgut to a level similar to that of WSSV-CN04 at 4 hpi. These findings indicate that the truncation of VP24 may attenuate the peroral infectivity of WSSV-CN04, and therefore verify the important role of VP24 in WSSV per os infection. The online version of this article (10.1186/s13567-017-0492-8) contains supplementary material, which is available to authorized users.
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发表时间: 2014
期刊: PloS one
影响因子: 3.7
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DOI: 10.1007/s11262-016-1421-z
发表时间: 2017-04-01
期刊: VIRUS GENES
影响因子: 1.6
作者:
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发表时间: 2001-10-01
期刊: AQUACULTURE
影响因子: 4.5
作者:
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