Key Laboratory of Maricultural Organism Disease Control, Ministry of Agriculture, Qingdao KeyLaboratory of Mariculture Epidemiology and Biosecurity, Yellow Sea Fisheries Research Institute,Chinese Academy of Fishery Sciences, Qingdao 266071, China.
Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266237, China.
Viruses. 2019 Apr 24;11(4):383. doi: 10.3390/v11040383.
Haliotid herpesvirus-1 (HaHV-1) is the first identified gastropod herpesvirus, causing a highly lethal neurologic disease of abalone species. The genome of HaHV-1 has been sequenced, but the functions of the putative genes and their roles during infection are still poorly understood. In the present study, transcriptomic profiles of at 0, 24 and 60 h post injection (hpi) with HaHV-1 were characterized through high-throughput RNA sequencing. A total of 448 M raw reads were obtained and assembled into 2.08 × 10 unigenes with a mean length of 1486 bp and an N50 of 2455 bp. Although we detected increased HaHV-1 DNA loads and active viral expression at 24 hpi, this evidence was not linked to significant changes of host transcriptomic profiles between 0 and 24 hpi, whereas a rich immune-related gene set was over-expressed at 60 hpi. These results indicate that, at least at the beginning of HaHV-1 infection, the virus can replicate with no activation of the host immune response. We propose that HaHV-1 may evolve more effective strategies to modulate the host immune response and hide during replication, so that it could evade the immune surveillance at the early stage of infection.
鲍疱疹病毒 1(HaHV-1)是首个鉴定的腹足类疱疹病毒,可引起鲍鱼物种的高致死性神经系统疾病。HaHV-1 的基因组已被测序,但假定基因的功能及其在感染过程中的作用仍知之甚少。在本研究中,通过高通量 RNA 测序对感染 HaHV-1 后 0、24 和 60 h 的 进行了转录组特征分析。共获得 448 M 个原始读数,组装成 2.08×10 个 unigenes,平均长度为 1486 bp,N50 为 2455 bp。尽管我们在 24 hpi 时检测到 HaHV-1 DNA 载量增加和病毒的活跃表达,但这一证据与 0 至 24 hpi 之间宿主转录组谱的显著变化无关,而在 60 hpi 时,丰富的免疫相关基因集被过度表达。这些结果表明,至少在 HaHV-1 感染的早期,病毒可以在不激活宿主免疫反应的情况下复制。我们提出,HaHV-1 可能进化出更有效的策略来调节宿主的免疫反应并在复制过程中隐藏,从而使其能够在感染的早期阶段逃避免疫监视。