Heavy oil exposure suppresses antiviral activities in Japanese flounder Paralichthys olivaceus infected with viral hemorrhagic septicemia virus (VHSV)
Heavy oil exposure suppresses antiviral activities in Japanese flounder Paralichthys olivaceus infected with viral hemorrhagic septicemia virus (VHSV)
复制标题
重油暴露抑制感染病毒性出血性败血症病毒（VHSV）的牙鲆的抗病毒活性
DOI：
10.1016/j.fsi.2022.03.046
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Nakayama Kei
中科院分区：
文献类型：
--
作者：
Song Jun-Young;Kitamura Shin-Ichi;Oh Myung-Joo;Nakayama Kei
重油(HO)暴露和病毒感染的联合治疗导致牙鲆(Paralichthys Olivaceus)死亡率增加。在这项研究中，我们研究了HO暴露如何影响日本比目鱼的免疫系统，特别是抗病毒活性。这些鱼被感染了病毒性出血性败血症病毒(VHSV)，然后暴露在HO中。我们分析了存活的鱼心脏中的病毒滴度和肾脏中的mRNA表达。暴露在重油中的鱼的病毒滴度高于发病阈值。结果表明，暴露于HO可能允许VHSV的复制，导致联合治疗组的死亡率更高。基因表达谱显示，联合治疗组的抗病毒活性相关基因，如干扰素和细胞凋亡诱导基因的表达低于单纯VHSV感染组。这些结果有助于解释在这两种应激源处理的鱼中出现高病毒滴度的原因。因此，在没有HO暴露的VHSV感染鱼中，病毒感染细胞中干扰素的产生和自然杀伤细胞诱导的细胞凋亡正常工作，但这些抗病毒活性被HO暴露略有抑制，可能导致病毒在宿主细胞中的广泛复制和VHS的发生。
A combined treatment of heavy oil (HO) exposure and virus infection induces increased mortality in Japanese flounder (Paralichthys olivaceus). In this study, we addressed how HO exposure affects the immune system, especially antiviral activities, in Japanese flounder. The fish were infected with viral hemorrhagic septicemia virus (VHSV), followed by exposure to HO. We analyzed virus titers in the heart and mRNA expression in the kidney of surviving fish. The virus titers in fish exposed to heavy oil were higher than the threshold for onset. The results suggest that HO exposure may allow the replication of VHSV, leading to higher mortality in the co-treated group. Gene-expression profiling demonstrated that the expression of antiviral-activity-related genes, such as those for interferon and apoptosis induction, were lower in the co-treated group than in the group with VHSV infection only. These results helped explain the high virus titers in fish treated with both stressors. Thus, interferon production in the virus-infected cells and apoptosis induction by natural killer cells worked normally in the VHSV-infected fish without HO exposure, but these antiviral activities were slightly suppressed by HO exposure, possibly leading to extensive viral replication in the host cells and the occurrence of VHS.