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FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication
The RIG-I-like receptor signaling pathway is crucial for producing type I interferon (IFN-I) against RNA viruses. The present study observed that viral infection increased annexin-A1 (ANXA1) expression, and ANXA1 then promoted RNA virus-induced IFN-I production. Compared to ANXA1 wild-type cells, AN...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Society for Microbiology
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9215249/ https://www.ncbi.nlm.nih.gov/pubmed/35604142 http://dx.doi.org/10.1128/jvi.00317-22 |
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author | Ma, XuSheng Zhang, KeShan Luo, ZhiKuan Nian, XiaoFeng Choudhury, S. K. Mohiuddin Zhu, ZiXiang Song, Rui Pei, JingJing Huo, YanLi Li, YuanYuan Yang, Fan Cao, WeiJun Liu, HuiSheng Liu, XiangTao Zheng, HaiXue |
author_facet | Ma, XuSheng Zhang, KeShan Luo, ZhiKuan Nian, XiaoFeng Choudhury, S. K. Mohiuddin Zhu, ZiXiang Song, Rui Pei, JingJing Huo, YanLi Li, YuanYuan Yang, Fan Cao, WeiJun Liu, HuiSheng Liu, XiangTao Zheng, HaiXue |
author_sort | Ma, XuSheng |
collection | PubMed |
description | The RIG-I-like receptor signaling pathway is crucial for producing type I interferon (IFN-I) against RNA viruses. The present study observed that viral infection increased annexin-A1 (ANXA1) expression, and ANXA1 then promoted RNA virus-induced IFN-I production. Compared to ANXA1 wild-type cells, ANXA1(−/−) knockout cells showed IFN-β production decreasing after viral stimulation. RNA virus stimulation induced ANXA1 to regulate IFN-β production through the TBK1-IRF3 axis but not through the NF-κB axis. ANXA1 also interacted with JAK1 and STAT1 to increase signal transduction induced by IFN-β or IFN-γ. We assessed the effect of ANXA1 on the replication of foot-and-mouth disease virus (FMDV) and found that ANXA1 inhibits FMDV replication dependent on IFN-I production. FMDV 3A plays critical roles in viral replication and host range. The results showed that FMDV 3A interacts with ANXA1 to inhibit its ability to promote IFN-β production. We also demonstrated that FMDV 3A inhibits the formation of ANXA1-TBK1 complex. These results indicate that ANXA1 positively regulates RNA virus-stimulated IFN-β production and FMDV 3A antagonizes ANXA1-promoted IFN-β production to modulate viral replication. IMPORTANCE FMDV is a pathogen that causes one of the world’s most destructive and highly contagious animal diseases. The FMDV 3A protein plays a critical role in viral replication and host range. Although 3A is one of the viral proteins that influences FMDV virulence, its underlying mechanisms remain unclear. ANXA1 is involved in immune activation against pathogens. The present study demonstrated that FMDV increases ANXA1 expression, while ANXA1 inhibits FMDV replication. The results also showed that ANXA1 promotes RNA virus-induced IFN-I production through the IRF3 axis at VISA and TBK1 levels. ANXA1 was also found to interact with JAK1 and STAT1 to strengthen signal transduction induced by IFN-β and IFN-γ. 3A interacted with ANXA1 to inhibit ANXA1-TBK1 complex formation, thereby antagonizing the inhibitory effect of ANXA1 on FMDV replication. This study helps to elucidate the mechanism underlying the effect of the 3A protein on FMDV replication. |
format | Online Article Text |
id | pubmed-9215249 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | American Society for Microbiology |
record_format | MEDLINE/PubMed |
spelling | pubmed-92152492022-06-23 FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication Ma, XuSheng Zhang, KeShan Luo, ZhiKuan Nian, XiaoFeng Choudhury, S. K. Mohiuddin Zhu, ZiXiang Song, Rui Pei, JingJing Huo, YanLi Li, YuanYuan Yang, Fan Cao, WeiJun Liu, HuiSheng Liu, XiangTao Zheng, HaiXue J Virol Pathogenesis and Immunity The RIG-I-like receptor signaling pathway is crucial for producing type I interferon (IFN-I) against RNA viruses. The present study observed that viral infection increased annexin-A1 (ANXA1) expression, and ANXA1 then promoted RNA virus-induced IFN-I production. Compared to ANXA1 wild-type cells, ANXA1(−/−) knockout cells showed IFN-β production decreasing after viral stimulation. RNA virus stimulation induced ANXA1 to regulate IFN-β production through the TBK1-IRF3 axis but not through the NF-κB axis. ANXA1 also interacted with JAK1 and STAT1 to increase signal transduction induced by IFN-β or IFN-γ. We assessed the effect of ANXA1 on the replication of foot-and-mouth disease virus (FMDV) and found that ANXA1 inhibits FMDV replication dependent on IFN-I production. FMDV 3A plays critical roles in viral replication and host range. The results showed that FMDV 3A interacts with ANXA1 to inhibit its ability to promote IFN-β production. We also demonstrated that FMDV 3A inhibits the formation of ANXA1-TBK1 complex. These results indicate that ANXA1 positively regulates RNA virus-stimulated IFN-β production and FMDV 3A antagonizes ANXA1-promoted IFN-β production to modulate viral replication. IMPORTANCE FMDV is a pathogen that causes one of the world’s most destructive and highly contagious animal diseases. The FMDV 3A protein plays a critical role in viral replication and host range. Although 3A is one of the viral proteins that influences FMDV virulence, its underlying mechanisms remain unclear. ANXA1 is involved in immune activation against pathogens. The present study demonstrated that FMDV increases ANXA1 expression, while ANXA1 inhibits FMDV replication. The results also showed that ANXA1 promotes RNA virus-induced IFN-I production through the IRF3 axis at VISA and TBK1 levels. ANXA1 was also found to interact with JAK1 and STAT1 to strengthen signal transduction induced by IFN-β and IFN-γ. 3A interacted with ANXA1 to inhibit ANXA1-TBK1 complex formation, thereby antagonizing the inhibitory effect of ANXA1 on FMDV replication. This study helps to elucidate the mechanism underlying the effect of the 3A protein on FMDV replication. American Society for Microbiology 2022-05-23 /pmc/articles/PMC9215249/ /pubmed/35604142 http://dx.doi.org/10.1128/jvi.00317-22 Text en Copyright © 2022 Ma et al. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Pathogenesis and Immunity Ma, XuSheng Zhang, KeShan Luo, ZhiKuan Nian, XiaoFeng Choudhury, S. K. Mohiuddin Zhu, ZiXiang Song, Rui Pei, JingJing Huo, YanLi Li, YuanYuan Yang, Fan Cao, WeiJun Liu, HuiSheng Liu, XiangTao Zheng, HaiXue FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication |
title | FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication |
title_full | FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication |
title_fullStr | FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication |
title_full_unstemmed | FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication |
title_short | FMDV 3A Antagonizes the Effect of ANXA1 to Positively Modulate Viral Replication |
title_sort | fmdv 3a antagonizes the effect of anxa1 to positively modulate viral replication |
topic | Pathogenesis and Immunity |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9215249/ https://www.ncbi.nlm.nih.gov/pubmed/35604142 http://dx.doi.org/10.1128/jvi.00317-22 |
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