Host–virus immune crosstalk and immune evasion mechanisms of African swine fever virus: recent progress and translational implications
- 1College of Veterinary Medicine, National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University
- 2Virology and Cell Technology Research Team, National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency (NSTDA)
Abstract
African swine fever (ASF), caused by African swine fever virus (ASFV), is an acute and highly contagious disease characterized by high fatality and rapid transmission and poses severe threats to the global pig industry. As a complex nucleocytoplasmic large DNA virus (NCLDV), ASFV has evolved sophisticated and highly efficient immune evasion strategies. It remodels the host immune microenvironment through multiple molecular mechanisms, inhibiting both innate and adaptive immune surveillance to sustained intracellular replication. Such potent immune evasion capacity constitutes the primary bottleneck restricting the development of safe and effective commercial vaccines. In this review, we summarize recent research progress and systematically delineate host innate and adaptive immune networks during ASFV infection. This review focuses on the core immune evasion mechanisms of ASFV, including the suppression of type I interferon production by antagonizing pattern recognition receptors (such as cGAS-STING and Toll-like receptor cascades) and the Janus kinase-signal transducer and activator of transcription (JAK-STAT) axis, the bidirectional regulation of nuclear factor kappa B (NF-κB) signaling and the NLR family pyrin domain containing 3 (NLRP3) inflammasome to manipulate inflammatory responses and programmed cell death, and the impairment of antigen presentation and lymphocyte activation. Moreover, this review elaborates on the temporal dynamics and synergistic effects of these immune evasion mechanisms, aiming to provide systematic theoretical insights into deciphering ASFV pathogenesis and facilitating novel vaccine development and anti-ASFV drug discovery.
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BibTeX
@article{he2026hostvirus,
title = {{Host–virus immune crosstalk and immune evasion mechanisms of African swine fever virus: recent progress and translational implications}},
author = {Xinglin He and Hong Li and Pengfei Li and Guiqian Wang and Yumei Sun and Xuexiang Yu and Guiqing Peng and Anan Jongkaewwattana and Qigai He and Wentao Li},
journal = {Animal Diseases},
year = {2026},
month = nov,
doi = {10.1186/s44149-026-00267-1},
url = {https://doi.org/10.1186/s44149-026-00267-1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Host–virus immune crosstalk and immune evasion mechanisms of African swine fever virus: recent progress and translational implications
AU - Xinglin He
AU - Hong Li
AU - Pengfei Li
AU - Guiqian Wang
AU - Yumei Sun
AU - Xuexiang Yu
AU - Guiqing Peng
AU - Anan Jongkaewwattana
AU - Qigai He
AU - Wentao Li
PY - 2026
DA - 2026/11/08
JO - Animal Diseases
DO - 10.1186/s44149-026-00267-1
UR - https://doi.org/10.1186/s44149-026-00267-1
AB - African swine fever (ASF), caused by African swine fever virus (ASFV), is an acute and highly contagious disease characterized by high fatality and rapid transmission and poses severe threats to the global pig industry. As a complex nucleocytoplasmic large DNA virus (NCLDV), ASFV has evolved sophisticated and highly efficient immune evasion strategies. It remodels the host immune microenvironment through multiple molecular mechanisms, inhibiting both innate and adaptive immune surveillance to sustained intracellular replication. Such potent immune evasion capacity constitutes the primary bottleneck restricting the development of safe and effective commercial vaccines. In this review, we summarize recent research progress and systematically delineate host innate and adaptive immune networks during ASFV infection. This review focuses on the core immune evasion mechanisms of ASFV, including the suppression of type I interferon production by antagonizing pattern recognition receptors (such as cGAS-STING and Toll-like receptor cascades) and the Janus kinase-signal transducer and activator of transcription (JAK-STAT) axis, the bidirectional regulation of nuclear factor kappa B (NF-κB) signaling and the NLR family pyrin domain containing 3 (NLRP3) inflammasome to manipulate inflammatory responses and programmed cell death, and the impairment of antigen presentation and lymphocyte activation. Moreover, this review elaborates on the temporal dynamics and synergistic effects of these immune evasion mechanisms, aiming to provide systematic theoretical insights into deciphering ASFV pathogenesis and facilitating novel vaccine development and anti-ASFV drug discovery.
SN - 2731-0442
ER -