生物学杂志 ›› 2022, Vol. 39 ›› Issue (3): 18-.doi: 10.3969/j.issn.2095-1736.2022.03.018

• 病毒学专题 • 上一篇    下一篇

WSSV和DIV1感染凡纳滨对虾对血淋巴凝固的影响

  

  1. 1. 中山大学 海洋科学学院, 珠海 519082; 2. 中山大学 生命科学学院, 广州 510275;
    3. 南方海洋科学与工程广东省实验室(珠海), 珠海 519082;
    4. 岭南现代农业科学与技术广东省实验室茂名分中心, 茂名 525099
  • 出版日期:2022-06-18 发布日期:2022-06-17
  • 通讯作者: 尹斌,博士,研究方向为对虾抗病育种,E-mail: yinb5@mail.sysu.edu.cn;李朝政,博士,教授,研究方向为对虾病害分子生物学,E-mail: lichzh5@mail.sysu.edu.cn
  • 作者简介:严栩蘅,硕士,研究方向为对虾病害分子生物学,E-mail: yanxh26@mail2.sysu.edu.cn
  • 基金资助:
    国家自然科学基金优秀青年基金项目(32022085); 国家自然科学基金重点项目(31930113); 岭南现代农业科学与技术广东省实验室茂名分中心自主研发项目(2021ZZ007); 南方海洋科学与工程广东省实验室(珠海)自主研发项目(SML2021SP301)

Effects of WSSV and DIV1 infection on hemolymph coagulation in Litopenaeus vannamei

  1. 1. School of Marine Sciences, Sun Yat-sen University, Zhuhai 519082, China; 2. School of Life Sciences,
    Sun Yat-sen University, Guangzhou 510275, China; 3. Southern Marine Science and Engineering Guangdong
    Laboratory(Zhuhai), Zhuhai 519082, China; 4.Maoming Branch, Guangdong Laboratory for Lingnan Modern
    Agriculture, Maoming 525099, China
  • Online:2022-06-18 Published:2022-06-17

摘要: 研究发现白斑综合征病毒(white spot syndrome virus,WSSV)和十足类虹彩病毒 1(decapod iridescent virus 1,DIV1)感染凡纳滨对虾(Litopenaeus vannamei)会抑制血淋巴的凝固。为了探究对虾凝血相关基因在抵御病毒感染过程中的作用,使用qPCR检测凡纳滨对虾凝血相关基因LvTGI、LvTGII和LvCP在两种病毒感染后的表达量差异,研究这些基因与病毒感染的互作关系;通过RNAi敲降LvTGI和LvTGII,分析它们在血淋巴凝结及宿主抗病毒免疫中的作用。结果显示,凝血系统关键基因LvTGI、LvTGII和LvCP在WSSV和DIV1感染后在不同组织中的表达模式存在显著差异,表明这些基因能够响应两种病毒的感染。RNAi敲降LvTGI和LvTGII后,对虾血淋巴凝固受到显著抑制,并且感染WSSV和DIV1的对虾累积死亡率较对照组明显增加,提示血淋巴凝固可能在抵抗两种病毒感染过程中发挥重要作用。研究结果为深入探讨对虾凝血系统与病毒的互作关系提供了重要参考信息。

关键词: 凡纳滨对虾, 血淋巴凝固, 白斑综合征病毒, 十足类虹彩病毒1, 抗病毒免疫

Abstract: The hemolymph coagulation was inhibited after white spot syndrome virus (WSSV) and decapod iridescent virus 1 (DIV1) infection in Litopenaeus vannamei. In this study, the role of clotting reaction genes in antiviral immunity was investigated. The expression of LvTGI, LvTGII and LvCP was assessed by qPCR after virus-stimulated to explore the interaction between clotting reaction genes and virus infection. RNAi was performed to further explore the function of LvTGI and LvTGII in antiviral immunity. It showed that the expression of LvTGI, LvTGII and LvCP could respond to WSSV and DIV1 infection, which were induced or inhibited in gills and hepatopancreas. Besides, knockdown of LvTGI and LvTGII by RNAi suppressed shrimp hemolymph coagulation, indicating that LvTGI and LvTGII play an important role in the clotting system. Silencing of LvTGI and LvTGII resulted in a higher cumulative mortality observed in virus infected shrimp, thus rendering shrimp more susceptibility to WSSV and DIV1. These results provided some insights into the interplay between the coagulation system and viral infection in shrimp.

Key words: Litopenaeus vannamei, hemolymph coagulation, WSSV, DIV1, antiviral immunity

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