Next Article in Journal
Cross-Species Transmission of Swine Hepatitis E Virus Genotype 3 to Rabbits
Next Article in Special Issue
Infection of Human Tracheal Epithelial Cells by H5 Avian Influenza Virus Is Regulated by the Acid Stability of Hemagglutinin and the pH of Target Cell Endosomes
Previous Article in Journal
Pseudorabies Virus UL24 Abrogates Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Degrading P65
Open AccessArticle

The R251K Substitution in Viral Protein PB2 Increases Viral Replication and Pathogenicity of Eurasian Avian-like H1N1 Swine Influenza Viruses

by Mengkai Cai 1,2, Ruting Zhong 1,3, Chenxiao Qin 1,2, Zhiqing Yu 1,2, Xiaoyan Wen 1,2, Junsi Xian 1,2, Yongjie Chen 1,2, Yu Cai 1,2, Heyou Yi 1,2, Lang Gong 1,2,* and Guihong Zhang 1,2,*
1
College of Veterinary Medicine, South China Agricultural University, Guangzhou 510462, China
2
Key Laboratory of Zoonosis Prevention and Control of Guangdong Province, South China Agricultural University, Guangzhou 510462, China
3
National Engineering Research Center for Breeding Swine Industry, South China Agricultural University, Guangzhou 510462, China
*
Authors to whom correspondence should be addressed.
Viruses 2020, 12(1), 52; https://doi.org/10.3390/v12010052
Received: 27 November 2019 / Revised: 29 December 2019 / Accepted: 31 December 2019 / Published: 2 January 2020
(This article belongs to the Special Issue Evolution and Pathogenesis of Avian and Animal Influenza Viruses)
The Eurasian avian-like swine (EA) H1N1 virus has affected the Chinese swine industry, and human infection cases have been reported occasionally. However, little is known about the pathogenic mechanism of EA H1N1 virus. In this study, we compared the mouse pathogenicity of A/swine/Guangdong/YJ4/2014 (YJ4) and A/swine/Guangdong/MS285/2017 (MS285) viruses, which had similar genotype to A/Hunan/42443/2015 (HuN-like). None of the mice inoculated with 106 TCID50 of YJ4 survived at 7 days post infection, while the survival rate of the MS285 group was 100%. Therefore, a series of single fragment reassortants in MS285 background and two rescued wild-type viruses were generated by using the reverse genetics method, and the pathogenicity analysis revealed that the PB2 gene contributed to the high virulence of YJ4 virus. Furthermore, there were 11 amino acid differences in PB2 between MS285 and YJ4 identified by sequence alignment, and 11 single amino acid mutant viruses were generated in the MS285 background. We found that the R251K mutation significantly increased the virulence of MS285 in mice, contributed to high polymerase activity and enhanced viral genome transcription and replication. These results indicate that PB2-R251K contributes to the virulence of the EA H1N1 virus and provide new insight into future molecular epidemiological surveillance strategies. View Full-Text
Keywords: Eurasian avian-like H1N1 swine influenza viruses; PB2 gene; PB2-R251K; pathogenicity; polymerase Eurasian avian-like H1N1 swine influenza viruses; PB2 gene; PB2-R251K; pathogenicity; polymerase
Show Figures

Figure 1

MDPI and ACS Style

Cai, M.; Zhong, R.; Qin, C.; Yu, Z.; Wen, X.; Xian, J.; Chen, Y.; Cai, Y.; Yi, H.; Gong, L.; Zhang, G. The R251K Substitution in Viral Protein PB2 Increases Viral Replication and Pathogenicity of Eurasian Avian-like H1N1 Swine Influenza Viruses. Viruses 2020, 12, 52.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop