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

Qingxin Meng; Pengtao Jiao; Lei Sun; Dayan Wang; Tingrong Luo; Wenhui Fan; Wenjun Liu

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

Author: Qingxin MENG ¹ ; Pengtao JIAO ² ; Lei SUN ² ; Dayan WANG ³ ; Tingrong LUO ¹ ; Wenhui FAN ² ; Wenjun LIU ¹
Author Information

1. Animal Science and Technology College, Guangxi University, Nanning 530004, Guangxi, China.
2. Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
3. Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Publication Type:Journal Article
Keywords: Victoria lineage; animal model; genetic analysis; influenza B virus; pathogenicity
MeSH: Amino Acids/genetics*; Animals; Antiviral Agents/pharmacology*; China; Cytokines/metabolism*; Hemagglutinins/metabolism*; Humans; Influenza B virus/pathogenicity*; Influenza, Human/virology*; Mice; Neuraminidase/genetics*; Orthomyxoviridae Infections/virology*; Phylogeny; RNA, Messenger/metabolism*; Virulence/genetics*
From: Chinese Journal of Biotechnology 2022;38(9):3390-3405
CountryChina
Language:Chinese
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 LD₅₀ was 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.