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Transcriptomic analysis reveals bovine herpesvirus 1 infection regulates innate immune response resulted in restricted viral replication in neuronal cells

文献类型： 外文期刊

作者： Jiang, Bo 1 ; Cao, Mengyao 1 ; Zhou, Linyi 1 ; Zhen, Hongyue 1 ; Cheng, Jing 1 ; Jinqiang, Cui 1 ; Liu, Wenxiao 1 ; Li, Yongqing 1 ;

作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing 100097, Peoples R China

2.Beijing Univ Agr, Coll Anim Sci & Technol, Beijing 102206, Peoples R China

3.Northeast Forestry Univ, Coll Anim Sci & Technol, Harbin 150000, Heilongjiang, Peoples R China

关键词： Bovine herpesvirus 1; RNA sequencing; Innate immune response; Neuronal cell; Latent infection

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.5； 五年影响因子：3.6 ）

ISSN： 0882-4010

年卷期： 2024 年 195 卷

页码：

收录情况： SCI

摘要： Background: Bovine herpesvirus 1 (BoHV-1) is a major pathogen that affects the global bovine population, primarily inducing respiratory and reproductive disorders. Its ability to establish latent infections in neuronal cells and to reactivate under certain conditions poses a continual threat to uninfected hosts. In this study, we aimed to analyze the replication characteristics of BoHV-1 in neuronal cells, as well as the effects of viral replication on host cell immunity and physiology. Methods: Using the Neuro-2a neuronal-origin cell line as a model, we explored the dynamics of BoHV-1 replication and analyzed differential gene expression profiles post-BoHV-1 infection using high-throughput RNA sequencing. Results: BoHV-1 demonstrated restricted replication in Neuro-2a cells. BoHV-1 induced apoptotic pathways and enhanced the transcription of interferon-stimulated genes and interferon regulatory factors while suppressing the complement cascade in Neuro-2a cells. Conclusions: Different from BoHV-1 infection in other non-highly differentiated somatic cells result in viral dominance, BoHV-1 regulated the innate immune response in neuronal cells formed a "virus-nerve cell" relative equilibrium state, which may account for the restricted replication of BoHV-1 in neuronal cells, leading to a latent infection. These findings provide a foundation for further research into the mechanism underlying BoHV1-induced latent infection in nerve cells.

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