Effect of Deletion of the Carboxyl Terminal of the NS1 Protein on Pathogenicity of the Influenza B Virus.
- Author:
Xue LI
;
Zhijun YU
;
Weiyang SUN
;
Qiang CHEN
;
Tiecheng WANG
;
Songtao YANG
;
Geng HUANG
;
Yuwei GAO
;
Xianzhu XIA
;
Xuemei ZHANG
- Publication Type:Journal Article
- MeSH:
Animals;
Body Weight;
Dogs;
Female;
HEK293 Cells;
Humans;
Influenza B virus;
genetics;
pathogenicity;
physiology;
Madin Darby Canine Kidney Cells;
Mice;
Mice, Inbred BALB C;
Sequence Deletion;
Survival Analysis;
Viral Load;
genetics;
Viral Nonstructural Proteins;
chemistry;
genetics;
Virulence
- From:
Chinese Journal of Virology
2015;31(4):404-409
- CountryChina
- Language:Chinese
-
Abstract:
To analyze the molecular basis of the variation of the pathogenicity of the influenza B virus, we rescued a recombinant virus with a deletion in the carboxyl terminal of the NS1 protein using reverse genetics based on the parental virus B-S9 of B/Yamagata/16/88. A mutant strain with a deletion of 171 amino acids in the carboxyl terminal of the NS1 protein was named "B-L5". BALB/c mice were inoculated with 3 X 105 EID50 of B-L5 and the parental virus B-S9, respectively. Then, weight changes, survival, and viral titers were documented. During 3 days post-inoculation (dpi) to 7 dpi, the weight of mice infected with B-S9 decreased. However, the weight of mice infected with B-L5 showed weight decreases only at 2 dpi, and quickly recovered at 3 dpi. B-S9 and B-L5 could replicate in the lungs of BALB/c mice. However, viral titers in the lungs of mice infected with B-L5 were 7900-times lower than those of mice infected with B-S9 at 3 dpi. Viral titers in the lungs of mice infected with B-L5 were not detected at 6 dpi. These results showed that, compared with the parent virus B-S9, the mutant virus B-L5 showed lower pathogenicity in BALB/c mice. Our study suggests that deletion of the carboxyl terminal of the NS1 protein decreases the pathogenicity of the influenza B virus. Establishment of a reverse-genetics system for the B influenza virus will provide a platform for studying its pathogenesis, and mechanism of transmission, and for developing live-attenuated influenza B virus vaccines.
