African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity

Abstract African swine fever virus (ASFV) causes acute and highly lethal disease in pigs. To counteract host defense systems and facilitate virus infection, many ASFV-encoded proteins have regulatory effects on the innate immune response. In this study, we constructed an MGF505-4R-deleted ASFV strai...

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Main Authors: Manman Yao, Pengfei Li, Xiangmin Li, Wentao Li, Ping Qian
Format: Article
Language:English
Published: BMC 2025-07-01
Series:Veterinary Research
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Online Access:https://doi.org/10.1186/s13567-025-01569-x
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author Manman Yao
Pengfei Li
Xiangmin Li
Wentao Li
Ping Qian
author_facet Manman Yao
Pengfei Li
Xiangmin Li
Wentao Li
Ping Qian
author_sort Manman Yao
collection DOAJ
description Abstract African swine fever virus (ASFV) causes acute and highly lethal disease in pigs. To counteract host defense systems and facilitate virus infection, many ASFV-encoded proteins have regulatory effects on the innate immune response. In this study, we constructed an MGF505-4R-deleted ASFV strain (ASFV-Δ4R) and found that, compared with the wild-type ASFV, ASFV-Δ4R infection significantly increased IFN-β production and elevated the mRNA levels of antiviral genes in porcine alveolar macrophages. Mechanistically, MGF505-4R interacts with cGAS and promotes its degradation by triggering Toll-interacting protein (TOLLIP)-mediated selective autophagy. Specifically, MGF505-4R enhanced the interaction between cGAS and TOLLIP, which subsequently led to increased degradation of cGAS. Additionally, MGF505-4R inhibited IFN-β-induced signal transmission by interacting with STAT1 and STAT2 and impeding their phosphorylation. This effect consequently prevented the formation of the ISGF3 heterotrimer and its subsequent translocation to the nucleus, leading to the downregulation of antiviral genes. As expected, compared with the ASFV-WT strain, ASFV-Δ4R infection increased phosphorylation of STAT1 and STAT2 and subsequent ISGF3 formation, leading to an elevated expression of antiviral gene ISGs. This discovery enhances the understanding of the immune regulation strategies evolved by ASFV and offers valuable perspectives for antiviral research targeting ASFV.
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institution Kabale University
issn 1297-9716
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publishDate 2025-07-01
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spelling doaj-art-3f7d09ddc9ab48f082debc5fcab1bad02025-08-20T03:37:40ZengBMCVeterinary Research1297-97162025-07-0156111910.1186/s13567-025-01569-xAfrican swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunityManman Yao0Pengfei Li1Xiangmin Li2Wentao Li3Ping Qian4National Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural UniversityNational Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural UniversityNational Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural UniversityNational Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural UniversityNational Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural UniversityAbstract African swine fever virus (ASFV) causes acute and highly lethal disease in pigs. To counteract host defense systems and facilitate virus infection, many ASFV-encoded proteins have regulatory effects on the innate immune response. In this study, we constructed an MGF505-4R-deleted ASFV strain (ASFV-Δ4R) and found that, compared with the wild-type ASFV, ASFV-Δ4R infection significantly increased IFN-β production and elevated the mRNA levels of antiviral genes in porcine alveolar macrophages. Mechanistically, MGF505-4R interacts with cGAS and promotes its degradation by triggering Toll-interacting protein (TOLLIP)-mediated selective autophagy. Specifically, MGF505-4R enhanced the interaction between cGAS and TOLLIP, which subsequently led to increased degradation of cGAS. Additionally, MGF505-4R inhibited IFN-β-induced signal transmission by interacting with STAT1 and STAT2 and impeding their phosphorylation. This effect consequently prevented the formation of the ISGF3 heterotrimer and its subsequent translocation to the nucleus, leading to the downregulation of antiviral genes. As expected, compared with the ASFV-WT strain, ASFV-Δ4R infection increased phosphorylation of STAT1 and STAT2 and subsequent ISGF3 formation, leading to an elevated expression of antiviral gene ISGs. This discovery enhances the understanding of the immune regulation strategies evolved by ASFV and offers valuable perspectives for antiviral research targeting ASFV.https://doi.org/10.1186/s13567-025-01569-xASFVMGF505-4RdegradationautolysosomecGAS-STINGimmune evasion
spellingShingle Manman Yao
Pengfei Li
Xiangmin Li
Wentao Li
Ping Qian
African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity
Veterinary Research
ASFV
MGF505-4R
degradation
autolysosome
cGAS-STING
immune evasion
title African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity
title_full African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity
title_fullStr African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity
title_full_unstemmed African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity
title_short African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity
title_sort african swine fever virus mgf505 4r facilitates cgas degradation through tollip mediated selective autophagy and inhibits the formation of isgf3 to evade innate immunity
topic ASFV
MGF505-4R
degradation
autolysosome
cGAS-STING
immune evasion
url https://doi.org/10.1186/s13567-025-01569-x
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