| Citation: |
XIAO Yu, WU Fan, ZHANG Baoshi, et al. The different regulatory effect of glycoproteins from virulent and attenuated strain of rabies virus on type I interferon signaling pathway[J]. Journal of South China Agricultural University, 2024, 45(2): 190-198. DOI: 10.7671/j.issn.1001-411X.202211015
|
Rabies is a highly lethal zoonotic infectious disease caused by rabies virus (RABV). Type I interferon (IFN-I) pathway plays an important role in resisting RABV infection. RABV can escape the antiviral effect of IFN-I through the function of its phosphoprotein and nucleoprotein. The aim of the study was to investigate the role of glycoprotein (G), which has an important impact on the pathogenicity of RABV, in regulating IFN-I pathway needs more comprehensive exploration.
This study replaced the G gene of the RABV attenuated strain Hep-Flury with the G gene of the pathogenic strain CVS-11 to rescue and acquire the recombinant virus HepG. We analyzed the differences in the activation and regulation of IFN-I pathway in vivo and in vitro infected with Hep-Flury, CVS-11 and HepG, and compared the differences of these virus strains in fighting against antiviral effect of IFN-I in nerve cells.
After replacing G gene, the recombinant virus HepG had enhanced pathogenicity, was able to kill 100% of mice and the proliferation level in the mouse brain was significantly higher than that of the parental strain Hep-Flury. While infecting mouse brain early and in vitro neuronal cells, the attenuated strain Hep-Flury was able to activate the expression of IFN-I pathway-related genes faster, and the activation ability of HepG was between that of Hep-Flury and CVS-11. After activation of the IFN-I pathway in neuronal cells using Poly(I:C), the proliferation of Hep-Flury was significantly inhibited, and the replication of CVS-11 and HepG was almost unaffected, showing some resistance.
G protein of RABV plays an important role in regulating and resisting the IFN-I pathway, providing the clue and evidence for further exploring how the G protein of RABV pathogenic strains helps the virus escape IFN-I pathway in the central nervous system.
| [1] |
SCOTT T P, NEL L H. Lyssaviruses and the fatal encephalitic disease rabies[J]. Frontiers in Immunology, 2021, 12: 786953. doi: 10.3389/fimmu.2021.786953.
|
| [2] |
FOOKS A R, BANYARD A C, HORTON D L, et al. Current status of rabies and prospects for elimination[J]. Lancet, 2014, 384(9951): 1389-1399. doi: 10.1016/S0140-6736(13)62707-5
|
| [3] |
扈荣良, 张守峰, 刘晔. 我国狂犬病预防和控制建议[J]. 中国人兽共患病学报, 2012, 28(5): 487-491. doi: 10.3969/j.issn.1002-2694.2012.05.020
|
| [4] |
FAUL E J, WANJALLA C N, SUTHAR M S, et al. Rabies virus infection induces type I interferon production in an IPS-1 dependent manner while dendritic cell activation relies on IFNAR signaling[J]. PLoS Pathogens, 2010, 6(7): e1001016. doi: 10.1371/journal.ppat.1001016
|
| [5] |
LI J, FABER M, DIETZSCHOLD B, et al. The role of toll-like receptors in the induction of immune responses during rabies virus infection[J]. Advances in Virus Research: Research Advances in Rabies, 2011, 79: 115-126.
|
| [6] |
LUO Z, LV L, LI Y, et al. Dual role of toll-like receptor 7 in the pathogenesis of rabies virus in a mouse model[J]. Journal of Virology, 2020, 94(9): e00111-20.
|
| [7] |
王林栋, 张守峰, 刘晔, 等. 基于RIG-I的狂犬病病毒免疫逃逸机制[J]. 中国生物制品学杂志, 2013, 26(10): 1517-1521. doi: 10.13200/j.cnki.cjb.001924
|
| [8] |
BRZOZKA K, FINKE S, CONZELMANN K K. Identification of the rabies virus alpha/beta interferon antagonist: Phosphoprotein P interferes with phosphorylation of interferon regulatory factor 3[J]. Journal of Virology, 2005, 79(12): 7673-7681. doi: 10.1128/JVI.79.12.7673-7681.2005
|
| [9] |
VIDY A, CHELBI-ALIX M, BLONDEL D. Rabies virus P protein interacts with STAT1 and inhibits interferon signal transduction pathways[J]. Journal of Virology, 2005, 79(22): 14411-14420. doi: 10.1128/JVI.79.22.14411-14420.2005
|
| [10] |
MASATANI T, ITO N, SHIMIZU K, et al. Rabies virus nucleoprotein functions to evade activation of the RIG-I-mediated antiviral response[J]. Journal of Virology, 2010, 84(8): 4002-4012. doi: 10.1128/JVI.02220-09
|
| [11] |
郭霄峰, 富振芳. 狂犬病毒糖蛋白基因的重排及病毒的拯救[J]. 华南农业大学学报, 2006, 27(1): 104-106. doi: 10.3969/j.issn.1001-411X.2006.01.027
|
| [12] |
ZHANG D, HE F, BI S, et al. Genome-wide transcriptional profiling reveals two distinct outcomes in central nervous system infections of rabies virus[J]. Frontiers in Microbiology, 2016, 7: 751. doi: 10.3389/fmicb.2016.00751.
|
| [13] |
HORNUNG V, ELLEGAST J, KIM S, et al. 5'-Triphosphate RNA is the ligand for RIG-I[J]. Science, 2006, 314(5801): 994-997. doi: 10.1126/science.1132505
|
| [14] |
YANG Y, HUANG Y, GNANADURAI C W, et al. The inability of wild-type rabies virus to activate dendritic cells is dependent on the glycoprotein and correlates with its low level of the de novo-synthesized leader RNA[J]. Journal of Virology, 2015, 89(4): 2157-2169. doi: 10.1128/JVI.02092-14
|
| [15] |
ZHANG H, HUANG J, SONG Y, et al. Regulation of innate immune responses by rabies virus[J]. Animal Models and Experimental Medicine, 2022, 5(5): 418-429. doi: 10.1002/ame2.12273
|
| 1. |
王丽亚，陈哲. 基于多特征融合的番茄叶片病害智能诊断系统开发. 电子制作. 2025(05): 41-45 .
| |
| 2. |
李文雪，孟洪兵，孙丽丽，韩璐宇. 融合多尺度注意力机制的棉花枯萎病识别算法研究. 现代农业装备. 2025(02): 86-92 .
| |
| 3. |
樊江川，王源桥，苟文博，蔡双泽，郭新宇，赵春江. 基于实例分割技术的草莓叶龄及冠幅表型快速提取方法. 智慧农业(中英文). 2024(02): 95-106 .
| |
| 4. |
李坤，刘婧，齐赫. 基于分层特征交叉注意力的小样本马铃薯病害叶片识别. 江苏农业科学. 2024(10): 210-216 .
| |
| 5. |
冯玉涵，孙剑，张志芳. 基于层间特征蒸馏网络的作物叶片病害检测. 中国农机化学报. 2024(09): 271-277 .
| |
| 6. |
李凤妹，龚青松，李奔奔，张敏，丁一，吕军. 基于改进YOLO v5s模型的水稻病虫害监测系统. 农业工程技术. 2024(20): 17-20 .
| |
| 7. |
杨欢，王钧，李广，吴江琪，谈燕. 大田环境下青贮玉米枯叶病检测模型. 软件导刊. 2024(09): 193-199 .
| |
| 8. |
方晓捷，严李强，张福豪，高心雨. 基于深度学习的农作物图像识别的发展. 江苏农业科学. 2024(20): 18-24 .
| |
| 9. |
麻剑钧，刘晓慈，金龙新，熊伟，易森林，封春芳，刘阳，夏先亮. 基于机器视觉的农作物病害识别研究进展. 湖南农业科学. 2023(09): 97-100 .
| |
| 10. |
郭文娟，冯全. 基于类激活映射的可解释性方法在农作物检测识别中的发展现状与趋势. 智能化农业装备学报(中英文). 2023(04): 41-48 .
|
Supported by: Beijing Renhe Information Technology Co., Ltd. 
DownLoad: