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Volume 17
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10.3390/v17020194
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This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Article

A Mutant of Africa Swine Fever Virus Protein p72 Enhances Antibody Production and Regulates the Production of Cytokines

by
Mingzhi Li
1,2,3,
Yihao Wang
1,2,3,
Quansheng Wang
1,2,3,
Lingdi Yang
1,2,3,
Shiguo Liu
1,2,3,
Guangzhi Li
3,
Ziqi Song
3,
Chulu Huang
3,
Lumei Kang
4,5,
Yanni Zhang
6,
Ting Wang
1,2,3,
Lingbao Kong
1,2,3,* and
Sha Li
1,2,3,*
1
Institute of Pathogenic Microorganism, Jiangxi Agricultural University, Nanchang 330000, China
2
Nanchang City Key Laboratory of Animal Virus and Genetic Engineering, Nanchang 330000, China
3
College of Bioscience and Engineering, Jiangxi Agricultural University, Nanchang 330000, China
4
College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330000, China
5
Center for Laboratory Animal Science, Nanchang University, Nanchang 330031, China
6
Jiangxi Province Center for Disease Control and Prevention, Nanchang 330029, China
*
Authors to whom correspondence should be addressed.
Viruses 2025, 17(2), 194; https://doi.org/10.3390/v17020194
Submission received: 11 December 2024 / Revised: 24 January 2025 / Accepted: 27 January 2025 / Published: 30 January 2025
(This article belongs to the Section Animal Viruses)
Versions Notes

Abstract

African swine fever virus (ASFV) is a severe threat to the global pig industry, and domestic pigs mostly develop severe clinical manifestations upon viral invasion. Currently, there is no available vaccine against ASFV. Its capsid structural protein p72 is one of the immuno-dominant proteins. In this study, we unexpectedly obtained a p72 mutant protein (p72∆377–428) which deleted the aa 377–428 within p72 and had stable and high expression in E. coli. Using SWISS-MODEL software, the prediction showed that p72∆377–428 was quite distinct from the wild-type p72 protein in structure. p72∆377–428 induced stronger antibody production in mice on day 42 and 56 post immunization and could recognize ASFV-infected swine sera. p72∆377–428 reduced IFN-γ production in the splenocytes from p72∆377–428-immunized mice and p72∆377–428-treated swine macrophages compared to p72. p72∆377–428 also decreased the production of pro-inflammatory cytokine genes, including IL-1β, IL-6, and IL-12, compared to p72 in mice. Further, we found that p72∆377–428 reduced the induction of pro-inflammatory cytokine genes by inhibiting AKT phosphorylation and HIF1α expression. Taken together, these findings have implications for immunological function and the corresponding mechanism of ASFV p72, and our study indicates that p72∆377–428 could serve as a novel candidate for ASFV vaccines and diagnostic reagents.
Keywords: ASFV p72; mutant; IFN-γ; HIF1α; AKT ASFV p72; mutant; IFN-γ; HIF1α; AKT

Share and Cite

MDPI and ACS Style

Li, M.; Wang, Y.; Wang, Q.; Yang, L.; Liu, S.; Li, G.; Song, Z.; Huang, C.; Kang, L.; Zhang, Y.; et al. A Mutant of Africa Swine Fever Virus Protein p72 Enhances Antibody Production and Regulates the Production of Cytokines. Viruses 2025, 17, 194. https://doi.org/10.3390/v17020194

AMA Style

Li M, Wang Y, Wang Q, Yang L, Liu S, Li G, Song Z, Huang C, Kang L, Zhang Y, et al. A Mutant of Africa Swine Fever Virus Protein p72 Enhances Antibody Production and Regulates the Production of Cytokines. Viruses. 2025; 17(2):194. https://doi.org/10.3390/v17020194

Chicago/Turabian Style

Li, Mingzhi, Yihao Wang, Quansheng Wang, Lingdi Yang, Shiguo Liu, Guangzhi Li, Ziqi Song, Chulu Huang, Lumei Kang, Yanni Zhang, and et al. 2025. "A Mutant of Africa Swine Fever Virus Protein p72 Enhances Antibody Production and Regulates the Production of Cytokines" Viruses 17, no. 2: 194. https://doi.org/10.3390/v17020194

APA Style

Li, M., Wang, Y., Wang, Q., Yang, L., Liu, S., Li, G., Song, Z., Huang, C., Kang, L., Zhang, Y., Wang, T., Kong, L., & Li, S. (2025). A Mutant of Africa Swine Fever Virus Protein p72 Enhances Antibody Production and Regulates the Production of Cytokines. Viruses, 17(2), 194. https://doi.org/10.3390/v17020194

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