PATHOGENICITY AND GENOMIC ANALYSES OF DENGUE VIRUS UNDER POSITIVE SELECTION IN HUMAN AND MOSQUITO CELLS
10.3969/j.issn.1005-0507.2022.01.003
- VernacularTitle:登革病毒在人与蚊虫细胞正选择压力下的致病性与基因序列变化分析
- Author:
Xiao-Juan ZHU
1
;
Yu-Ting JIANG
;
Heng-Duan ZHANG
;
Jian GAO
;
Zhi-Ming WU
;
Chun-Xiao LI
;
Yan-De DONG
;
Dan XING
;
Xiao-Xia GUO
;
Tong-Yan ZHAO
Author Information
1. 军事科学院军事医学研究院微生物流行病研究所,病原微生物生物安全国家重点实验室,北京市虫媒病与自然疫源性疾病重点实验室 北京100071
- Keywords:
Dengue-2 virus;
Alternating passage;
Nucleotide mutations;
Virulence
- From:
Acta Parasitologica et Medica Entomologica Sinica
2022;29(1):14-24
- CountryChina
- Language:Chinese
-
Abstract:
Dengue virus ( DENV ) perpetuates in an alternating cycle replication in arthropod and vertebrate hosts. It is particularly important to gain comprehensive understanding of host-virus interactions and the relationship between genetic variation and virulence. To simulate the transmit of DENN between human hosts and mosquito vectors, DENV was repeatedly passaged between human hepatocellular carcinoma cell line ( Huh-7) and mosquito cell line ( C6/36) . After 10 and 18 passages, the fitness of viral populations was measured with one-step growth curves and their virulence to mice and vector transmissibility were evaluated. Mutations in each population were determined by nucleotide sequencing. Viral fitness of DENV-2 decreased following alternating passages but increased after serial passages. Analysis of the amino acid sequences revealed that DENV that underwent continuous passage in C6/36 cells accumulated fewer mutations than virus passaged in Huh-7 cells or transferred between both cell types. Furthermore, the increased virulence that observed in serial passages might be due to the amino acid changes at positions 155 and 186 of protein E and the decreased virulence that observed in alternate passages might be due to the mutation at position 307. These results explored relationship between pathogenicity and genomic mutations of DENN and are valuable to guide the monitoring of future outbreaks.