Wei Mao-Le, Li Ya-Nan, Wang Jing-Li, Ma Cui-Ping, Kang Hui-Gang, Li Pei-Jun, Zhang Xiang, Huang Bo-Wen, Bai Chang-Ming
Sino-UAE International Cooperative Joint Laboratory of Pathogenic Microorganism Rapid Detection, Qingdao Nucleic Acid Rapid Detection Engineering Research Center, Qingdao Key Laboratory of Nucleic Acid Rapid Detection, College of Biological Engineering, Qingdao University of Science and Technology, Qingdao 266042, China.
State Key Laboratory of Mariculture Biobreeding and Sustainable Goods, Key Laboratory of Maricultural Organism Disease Control, Ministry of Agriculture, Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Qingdao 266071, China.
Biology (Basel). 2025 Jan 24;14(2):121. doi: 10.3390/biology14020121.
Haliotid herpesvirus 1 (HAHV-1) causes significant damage to the abalone aquaculture industry. Knowledge of HAHV-1 invasion and host defense mechanisms is limited due to the lack of stable molluscan cell lines. The present study established an infection model of HAHV-1 using the primary suspension cultures of hemocytes from and . The cytopathic effects of HAHV-1 on adherent-cultured hemocytes of both species were also investigated. The HAHV-1 DNA loads were firstly monitored by means of quantitative PCR during the development of viral infection, and subsequently the mechanism of interaction between HAHV-1 and hemocytes was explored by means of a transcriptome analysis. hemocytes exhibited a high degree of susceptibility to HAHV-1, with viral loads reaching a peak of 4.0 × 10⁷ copies/ng DNA. In contrast, no significant replication was observed in hemocytes. Transcriptome analysis revealed that HAHV-1 evades the host immune response in the early stages of infection, and hijacks the host's energy and redox metabolism to promote its replication at the late stages. Consequently, this study provides a valuable reference point for the investigation of virus-host interaction between HAHV-1 and abalone .
鲍疱疹病毒1型(HAHV-1)对鲍鱼养殖业造成了重大损害。由于缺乏稳定的软体动物细胞系,关于HAHV-1的入侵和宿主防御机制的了解有限。本研究利用来自[具体来源1]和[具体来源2]的血细胞原代悬浮培养物建立了HAHV-1感染模型。还研究了HAHV-1对这两个物种贴壁培养血细胞的细胞病变效应。在病毒感染过程中,首先通过定量PCR监测HAHV-1的DNA载量,随后通过转录组分析探索HAHV-1与血细胞之间的相互作用机制。[具体来源1]的血细胞对HAHV-1表现出高度易感性,病毒载量达到4.0×10⁷拷贝/ng DNA的峰值。相比之下,在[具体来源2]的血细胞中未观察到明显的复制。转录组分析表明,HAHV-1在感染早期逃避宿主免疫反应,并在后期劫持宿主的能量和氧化还原代谢以促进其复制。因此,本研究为研究HAHV-1与鲍鱼之间的病毒-宿主相互作用提供了有价值的参考点。