Decapod iridescent virus 1 (DIV1) 168L can target cuticle protein 8 from Litopenaeus vannamei

IF 3.6 3区 生物学 Q1 ZOOLOGY Journal of invertebrate pathology Pub Date : 2024-06-27 DOI:10.1016/j.jip.2024.108162
Qin Zheng , Huan-huan Rao , Fu-Rong Zhao, Xiao-Juan Chen, Wei Wang, Jian-Ming Chen
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Abstract

Decapod iridescent virus 1 (DIV1) stands as a significant pathogen affecting crustaceans, posing a grave threat to the shrimp industries in aquaculture dependent nations. Within the Iridoviridae family, the conserved envelope protein DIV1-168L plays a pivotal role in virion entry. Nonetheless, the host factors that interact with 168L remain unidentified. To address this gap, we established a cDNA library derived from Litopenaeus vannamei gill tissue and conducted yeast two-hybrid screening to identify host factors that interact with 168L. Additionally, we performed co-immunoprecipitation assays to verify the interaction between cuticle protein 8 (CP8) and 168L. Expression pattern analysis revealed the presence of CP8 transcripts in the gill and epidermis. Furthermore, immunohistochemistry results demonstrated the expression of CP8 in gill cells and its localization in the gill filament epithelium. Fluorescence analysis indicated that full-length CP8 colocalized with 168L in the cytoplasm of Sf9 cells. Removal of the signal peptide from the N-terminal of CP8 eliminated its concentration in the cytoplasm. Additionally, CP8 expression was significantly inhibited during DIV1 infection. Therefore, our research contributes to a better understanding of the entry mechanism of iridovirids.

The GenBank accession number for the DIV1 sequence is MF197913.1.

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底足虹彩病毒 1 (DIV1) 168L 能靶向万年青的角质层蛋白 8。
十足虹彩病毒 1(DIV1)是影响甲壳类动物的重要病原体,对依赖水产养殖的国家的对虾产业构成严重威胁。在虹彩病毒科中,保守的包膜蛋白 DIV1-168L 在病毒进入过程中起着关键作用。然而,与 168L 相互作用的宿主因子仍未确定。为了填补这一空白,我们建立了一个来自凡纳滨对虾鳃组织的 cDNA 文库,并进行了酵母双杂交筛选,以确定与 168L 相互作用的宿主因子。此外,我们还进行了共免疫沉淀试验,以验证角质层蛋白8(CP8)与168L之间的相互作用。表达模式分析显示,鳃和表皮中存在 CP8 转录本。此外,免疫组化结果表明 CP8 在鳃细胞中表达,并定位在鳃丝上皮细胞中。荧光分析表明,全长 CP8 与 168L 共同定位在 Sf9 细胞的细胞质中。去除 CP8 N 端的信号肽后,其在细胞质中的浓度消失。此外,在DIV1感染期间,CP8的表达受到了显著抑制。因此,我们的研究有助于更好地理解虹彩病毒的进入机制。DIV1序列的GenBank登录号为MF197913.1。
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来源期刊
CiteScore
6.10
自引率
5.90%
发文量
94
审稿时长
1 months
期刊介绍: The Journal of Invertebrate Pathology presents original research articles and notes on the induction and pathogenesis of diseases of invertebrates, including the suppression of diseases in beneficial species, and the use of diseases in controlling undesirable species. In addition, the journal publishes the results of physiological, morphological, genetic, immunological and ecological studies as related to the etiologic agents of diseases of invertebrates. The Journal of Invertebrate Pathology is the adopted journal of the Society for Invertebrate Pathology, and is available to SIP members at a special reduced price.
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