B型流感病毒B/Guangxi-Jiangzhou/1352/2018毒株的遗传进化及其对小鼠的致病性分析

doi:10.13345/j.cjb.220139

科微学术

生物工程学报

首页 > 过刊浏览>2022年第38卷第9期 >3390-3405. DOI:10.13345/j.cjb.220139

PDF HTML阅读 XML下载导出引用引用提醒

B型流感病毒B/Guangxi-Jiangzhou/1352/2018毒株的遗传进化及其对小鼠的致病性分析
DOI:
                        10.13345/j.cjb.220139
                    
CSTR:
                        32114.14.j.cjb.220139
                    
作者:
                        孟庆鑫孟庆鑫
广西大学 动物科学技术学院, 广西 南宁 530004;中国科学院微生物研究所 病原微生物与免疫学重点实验室, 北京 100101
在期刊界中查找
在百度中查找
在本站中查找
焦鹏涛焦鹏涛
中国科学院微生物研究所 病原微生物与免疫学重点实验室, 北京 100101
在期刊界中查找
在百度中查找
在本站中查找
孙蕾孙蕾
中国科学院微生物研究所 病原微生物与免疫学重点实验室, 北京 100101;中国科学院大学, 北京 100049
在期刊界中查找
在百度中查找
在本站中查找
王大燕王大燕
中国疾病预防控制中心, 北京 102206
在期刊界中查找
在百度中查找
在本站中查找
罗廷荣罗廷荣
广西大学 动物科学技术学院, 广西 南宁 530004
在期刊界中查找
在百度中查找
在本站中查找
范文辉范文辉
中国科学院微生物研究所 病原微生物与免疫学重点实验室, 北京 100101
在期刊界中查找
在百度中查找
在本站中查找
刘文军刘文军
广西大学 动物科学技术学院, 广西 南宁 530004;中国科学院微生物研究所 病原微生物与免疫学重点实验室, 北京 100101;中国科学院大学, 北京 100049
在期刊界中查找
在百度中查找
在本站中查找

                    
作者单位:
作者简介:
通讯作者:
中图分类号:
基金项目:国家自然科学基金（32070164）；中国科学院B类先导专项（XDB29010000）

Phylogenetic and pathogenicity analysis of influenza B virus strain B/Guangxi-Jiangzhou/1352/2018

Author:

MENG Qingxin
MENG Qingxin
Animal Science and Technology College, Guangxi University, Nanning 530004, Guangxi, China;Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China
在期刊界中查找
在百度中查找
在本站中查找
JIAO Pengtao
JIAO Pengtao
Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China
在期刊界中查找
在百度中查找
在本站中查找
SUN Lei
SUN Lei
Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China;University of Chinese Academy of Sciences, Beijing 100049, China
在期刊界中查找
在百度中查找
在本站中查找
WANG Dayan
WANG Dayan
Chinese Center for Disease Control and Prevention, Beijing 102206, China
在期刊界中查找
在百度中查找
在本站中查找
LUO Tingrong
LUO Tingrong
Animal Science and Technology College, Guangxi University, Nanning 530004, Guangxi, China
在期刊界中查找
在百度中查找
在本站中查找
FAN Wenhui
FAN Wenhui
Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China
在期刊界中查找
在百度中查找
在本站中查找
LIU Wenjun
LIU Wenjun
Animal Science and Technology College, Guangxi University, Nanning 530004, Guangxi, China;Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China;University of Chinese Academy of Sciences, Beijing 100049, China
在期刊界中查找
在百度中查找
在本站中查找

Affiliation:

Fund Project:

摘要

图/表

访问统计

参考文献 [42]

相似文献 [20]

引证文献

资源附件

文章评论

摘要:

B型流感病毒(influenza B virus,IBV)比A型流感病毒(influenza A virus,IAV)更易引发并发症，在一定季节内造成的疾病负担甚至超过IAV，但目前人们对IBV的关注较少。为了分析IBV临床毒株B/Guangxi-Jiangzhou/1352/2018的遗传进化特点，本研究构建了系统进化树，并以世界卫生组织推荐的疫苗株为参考，对其血凝素(hemagglutinin,HA)和神经氨酸酶(neuraminidase,NA)进行了氨基酸序列同源性及突变位点分析。分析结果发现B/Guangxi-Jiangzhou/1352/2018毒株无谱系间重配现象，与同年疫苗株B/Colorado/06/2017匹配性较差。另外，测定了B/Guangxi-Jiangzhou/1352/2018毒株感染小鼠的半数致死量(median lethal dose,LD₅₀)及其对小鼠的致病性。结果表明，B/Guangxi-Jiangzhou/1352/2018毒株感染小鼠的LD₅₀为10^5.9TCID₅₀(median tissue culture infective dose)，小鼠肺脏中病毒滴度在感染后1 d达到高峰，炎性细胞因子的mRNA水平在感染后12 h达到高峰，且感染后肺脏中的肺泡损伤严重，有大量炎性细胞浸润。本研究证明了IBV临床毒株B/Guangxi-Jiangzhou/1352/2018可以感染小鼠并诱发典型的肺脏炎症，为研究IBV致病及传播机制奠定了基础，为评价新型流感疫苗、抗病毒和抗炎症药物提供了理想的动物模型。

关键词:B型流感病毒;Victoria谱系;遗传进化分析;致病性;动物模型

Abstract:

Influenza B virus (IBV) is more likely to cause complications than influenza A virus (IAV) and even causes higher disease burden than IAV in a certain season, but IBV has received less attention. In order to analyze the genetic evolution characteristics of the clinical strain IBV (B/Guangxi- Jiangzhou/1352/2018), we constructed genetic evolution trees and analyzed the homology and different amino acids of hemagglutinin and neuraminidase referring to the vaccine strains recommended by World Health Organization (WHO). We found that strain B/Guangxi-Jiangzhou/1352/2018 was free of interlineage reassortment and poorly matched with the vaccine strain B/Colorado/06/2017 of the same year. We also determined the median lethal dose (LD₅₀) and the pathogenicity of strain B/Guangxi-Jiangzhou/1352/2018 in mice. The results showed that the LD₅₀was 10^5.9 TCID₅₀(median tissue culture infective dose), the IBV titer in the lungs reached peak 1 d post infection and the mRNA level of the most of inflammatory cytokines in the lungs reached peak 12 h post infection. The alveoli in the lungs were severely damaged and a large number of inflammatory cells were infiltrated post infection. The study demonstrated that the clinical strain IBV (B/Guangxi-Jiangzhou/1352/2018) could infect mice and induce typical lung inflammation. This will facilitate the research on the pathogenesis and transmission mechanism of IBV, and provide an ideal animal model for evaluation of new vaccines, antiviral and anti-inflammatory drug.

Key words:influenza B virus;Victoria lineage;genetic analysis;pathogenicity;animal model

参考文献

[1] Hause BM, Collin EA, Liu RX, et al. Characterization of a novel influenza virus in cattle and swine:proposal for a new genus in the Orthomyxoviridae family. mBio, 2014, 5(2):e00031-14.

[2] Smith DB, Gaunt ER, Digard P, et al. Detection of influenza C virus but not influenza D virus in Scottish respiratory samples. J Clin Virol, 2016, 74:50-53.

[3] Moussi AE, Pozo F, Kacem MABH, et al. Virological surveillance of influenza viruses during the 2008-09, 2009-10 and 2010-11 seasons in Tunisia. PLoS One, 2013, 8(9):e74064.

[4] Osterhaus AD, Rimmelzwaan GF, Martina BE, et al. Influenza B virus in seals. Science, 2000, 288(5468):1051-1053.

[5] Ramis AJ, Van Riel D, Van De Bildt MWG, et al. Influenza A and B virus attachment to respiratory tract in marine mammals. Emerg Infect Dis, 2012, 18(5):817-820.

[6] McCullers JA, Hayden FG. Fatal influenza B infections:time to reexamine influenza research priorities. J Infect Dis, 2012, 205(6):870-872.

[7] Özkaya PY, Turanli EE, Metin H, et al. Severe influenza virus infection in children admitted to the PICU:comparison of influenza A and influenza B virus infection. J Med Virol, 2022, 94(2):575-581.

[8] Heikkinen T, Ikonen N, Ziegler T. Impact of influenza B lineage-level mismatch between trivalent seasonal influenza vaccines and circulating viruses, 1999‒2012. Clin Infect Dis, 2014, 59(11):1519-1524.

[9] 张瑶, 舒跃龙, 王大燕. B型流感病毒相关研究进展. 疾病监测, 2017, 32(2):153-156. Zhang Y, Shu YL, Wang DY. Progressin research of influenza B virus. Dis Surveillance, 2017, 32(2):153-156(in Chinese).

[10] Francis T Jr. A new type of virus from epidemic influenza. Science, 1940, 92(2392):405-408.

[11] Tafalla M, Buijssen M, Geets R, et al. A comprehensive review of the epidemiology and disease burden of Influenza B in 9 European countries. Hum Vaccin Immunother, 2016, 12(4):993-1002.

[12] 何兰, 何军, 俞俊岭, 等. 2017‒2018年安徽省乙型流感病毒病原学特征分析. 中华实验和临床病毒学杂志, 2018, 32(5):479-483. He L, He J, Yu JL, et al. Virological characteristics of influenza B virus isolated in Anhui province during 2017‒2018 surveillance year. Chin J Exp Clin Virol, 2018, 32(5):479-483(in Chinese).

[13] Lamb RA, Choppin PW. The gene structure and replication of influenza virus. Annu Rev Biochem, 1983, 52:467-506.

[14] Chen RB, Holmes EC. The evolutionary dynamics of human influenza B virus. J Mol Evol, 2008, 66(6):655-663.

[15] Dudas G, Bedford T, Lycett S, et al. Reassortment between influenza B lineages and the emergence of a coadapted PB1-PB2-HA gene complex. Mol Biol Evol, 2015, 32(1):162-172.

[16] Nerome R, Hiromoto Y, Sugita S, et al. Evolutionary characteristics of influenza B virus since its first isolation in 1940:dynamic circulation of deletion and insertion mechanism. Arch Virol, 1998, 143(8):1569-1583.

[17] McCullers JA, Wang GC, He S, et al. Reassortment and insertion-deletion are strategies for the evolution of influenza B viruses in nature. J Virol, 1999, 73(9):7343-7348.

[18] 杨子峰, 杨春光, 王玉涛, 等. 从乙型流感病毒流行株中筛选获得鼠肺适应株的研究. 第三军医大学学报, 2014, 36(5):446-449. Yang ZF, Yang CG, Wang YT, et al. Screening of mouse-lung adapted strain from clinical influenza B viruses. J Third Mil Med Univ, 2014, 36(5):446-449(in Chinese).

[19] 张海亮, 冯俊霞, 肖冬光, 等. B型流感病毒小鼠致死模型的建立. 军事医学, 2017, 41(1):53-57. Zhang HL, Feng JX, Xiao DG, et al. Establishment of a lethal mouse model of influenza B virus. Mil Med Sci, 2017, 41(1):53-57(in Chinese).

[20] Wang QH, Cheng F, Lu MY, et al. Crystal structure of unliganded influenza B virus hemagglutinin. J Virol, 2008, 82(6):3011-3020.

[21] Wang QH, Tian X, Chen XR, et al. Structural basis for receptor specificity of influenza B virus hemagglutinin. PNAS, 2007, 104(43):16874-16879.

[22] Lin YP, Gregory V, Bennett M, et al. Recent changes among human influenza viruses. Virus Res, 2004, 103(1/2):47-52.

[23] Liu Q, Zhou YH, Yang ZQ. The cytokine storm of severe influenza and development of immunomodulatory therapy. Cell Mol Immunol, 2016, 13(1):3-10.

[24] Shim JM, Kim J, Tenson T, et al. Influenza virus infection, interferon response, viral counter-response, and apoptosis. Viruses, 2017, 9(8):223.

[25] Jiang JW, Li J, Fan WH, et al. Robust Lys63-linked ubiquitination of RIG-I promotes cytokine eruption in early influenza B virus infection. J Virol, 2016, 90(14):6263-6275.

[26] Yang JR, Huang YP, Chang FY, et al. Phylogenetic and evolutionary history of influenza B viruses, which caused a large epidemic in 2011-2012, Taiwan. PLoS ONE, 2012, 7(10):e47179.

[27] Kanegae Y, Sugita S, Endo A, et al. Evolutionary pattern of the hemagglutinin gene of influenza B viruses isolated in Japan:cocirculating lineages in the same epidemic season. J Virol, 1990, 64(6):2860-2865.

[28] Kato-Miyashita S, Sakai-Tagawa Y, Yamashita M, et al. Antigenic variants of influenza B viruses isolated in Japan during the 2017‒2018 and 2018‒2019 influenza seasons. Influenza Other Respir Viruses, 2020, 14(3):311-319.

[29] Ilyushina NA, Lee N, Lugovtsev VY, et al. Adaptation of influenza B virus by serial passage in human airway epithelial cells. Virology, 2020, 549:68-76.

[30] Lugovtsev VY, Smith DF, Weir JP. Changes of the receptor-binding properties of influenza B virus B/Victoria/504/2000 during adaptation in chicken eggs. Virology, 2009, 394(2):218-226.

[31] Ni FY, Mbawuike IN, Kondrashkina E, et al. The roles of hemagglutinin Phe-95 in receptor binding and pathogenicity of influenza B virus. Virology, 2014, 450/451:71-83.

[32] Zhang Y, Wen LY, Zhao X, et al. Antigenic and genetic study of influenza virus B circulated in China in 2004‒2005. Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi, 2006, 20(2):11-13.

[33] 张烨, 温乐英, 赵翔, 等. 2004‒2005年中国B型流感病毒抗原性及基因特性研究. 中华实验和临床病毒学杂志, 2006(2):11-13. Zhang Y, Wen LY, Zhao X, et al. Antigenic and genetic study of influenza virus B circulated in China in 2004‒2005. Chin J Exp Clin Virol, 2006(2):11-13(in Chinese).

[34] Burnham AJ, Baranovich T, Govorkova EA. Neuraminidase inhibitors for influenza B virus infection:efficacy and resistance. Antiviral Res, 2013, 100(2):520-534.

[35] Burnham AJ, Armstrong J, Lowen AC, et al. Competitive fitness of influenza B viruses with neuraminidase inhibitor-resistant substitutions in a coinfection model of the human airway epithelium. J Virol, 2015, 89(8):4575-4587.

[36] Fujisaki S, Takashita E, Yokoyama M, et al. A single E105K mutation far from the active site of influenza B virus neuraminidase contributes to reduced susceptibility to multiple neuraminidase-inhibitor drugs. Biochem Biophys Res Commun, 2012, 429(1/2):51-56.

[37] Hai R, Martínez-Sobrido L, Fraser KA, et al. Influenza B virus NS₁-truncated mutants:live-attenuated vaccine approach. J Virol, 2008, 82(21):10580-10590.

[38] Lai C, Struckhoff JJ, Schneider J, et al. Mice lacking the ISG15 E1 enzyme UbE1L demonstrate increased susceptibility to both mouse-adapted and non-mouse-adapted influenza B virus infection. J Virol, 2009, 83(2):1147-1151.

[39] Van De Sandt CE, Bodewes R, Rimmelzwaan GF, et al. Influenza B viruses:not to be discounted. Future Microbiol, 2015, 10(9):1447-1465.

[40] Dai JP, Gu LM, Su Y, et al. Inhibition of curcumin on influenza A virus infection and influenzal pneumonia via oxidative stress, TLR2/4, p38/JNK MAPK and NF-κB pathways. Int Immunopharmacol, 2018, 54:177-187.

[41] Lenschow DJ, Lai C, Frias-Staheli N, et al. IFN -stimulated gene 15 functions as a critical antiviral molecule against influenza, Herpes, and Sindbis viruses. PNAS, 2007, 104(4):1371-1376.

[42] Woo PCY, Tung ETK, Chan KH, et al. Cytokine profiles induced by the novel swine-origin influenza A/H1N1 virus:implications for treatment strategies. J Infect Dis, 2010, 201(3):346-353.