Immune mechanisms induced by an HSV-1 mutant strain: Discrepancy analysis of the immune system gene profile in comparison with a wild-type strain
Immune mechanisms induced by an HSV-1 mutant strain: Discrepancy analysis of the immune system gene profile in comparison with a wild-type strain
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HSV-1突变株诱导的免疫机制：与野生型株相比免疫系统基因谱的差异分析
DOI：
10.1016/j.vaccine.2018.03.056
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发表时间：
2018-04-25
期刊：
影响因子：
5.5
通讯作者：
Li, Qihan
中科院分区：
文献类型：
--
作者：
Zhang, Xiaolong;Jiang, Quanlong;Li, Qihan
单纯疱疹病毒是一种流行于不同年龄段人群的病原体。目前还没有预防性或治疗性疫苗，这一事实表明有必要进一步研究该病毒和各种候选疫苗诱导的免疫机制。我们之前产生了HSV-1突变株M3，在ul7、ul41和LAT中有部分缺失，在小鼠中产生了减弱的表型。在本研究中，我们进行了一项比较分析，以表征M3和野生型HSV-1在小鼠模型中诱导的免疫反应。感染野生型HSV-1可引起炎症为主的反应和适应性免疫抑制，并伴有严重的病理损害。相比之下，感染M3诱导了系统的免疫反应，包括充分激活天然免疫和获得性免疫，并且没有明显的病理变化。此外，M3诱导的免疫反应保护小鼠免受HSV-1野生型毒株的致命攻击，并抑制病毒增殖和损害潜伏期。这些数据对使用突变株构建策略进一步开发HSV-1疫苗是有用的。(C)2018爱思唯尔有限公司。保留所有权利。
Herpes simplex virus is a prevalent pathogen of humans of various age groups. The fact that no prophylactic or therapeutic vaccine is currently available suggests a significant need to further investigate the immune mechanisms induced by the virus and various vaccine candidates. We previously generated an HSV-1 mutant strain, M3, with partial deletions in ul7, ul41 and LAT that produced an attenuated phenotype in mice. In the present study, we performed a comparative analysis to characterize the immune responses induced by M3 versus wild-type HSV-1 in a mouse model. Infection with wild-type HSV-1 triggered an inflammatory-dominated response and adaptive immunity suppression and was accompanied by severe pathological damage. In contrast, infection with M3 induced a systematic immune response involving full activation of both innate and adaptive immunity and was accompanied by no obvious pathological changes. Furthermore, the immune response induced by M3 protected mice from lethal challenge with wild -type strains of HSV-1 and restrained virus proliferation and impaired latency. These data are useful for further HSV-1 vaccine development using a mutant strain construction strategy. (C) 2018 Elsevier Ltd. All rights reserved.