Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation
Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection, resulting in great economic losses. Although ALV-J-induced immunosuppression has been well established, the underlying molecular mechanism for such ind...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2018-05-01
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| Series: | Frontiers in Microbiology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fmicb.2018.01089/full |
| _version_ | 1818549168241639424 |
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| author | Wencheng Lin Wencheng Lin Wencheng Lin Zhouyi Xu Yiming Yan Huanmin Zhang Hongxin Li Hongxin Li Hongxin Li Weiguo Chen Weiguo Chen Weiguo Chen Feng Chen Feng Chen Feng Chen Qingmei Xie Qingmei Xie Qingmei Xie |
| author_facet | Wencheng Lin Wencheng Lin Wencheng Lin Zhouyi Xu Yiming Yan Huanmin Zhang Hongxin Li Hongxin Li Hongxin Li Weiguo Chen Weiguo Chen Weiguo Chen Feng Chen Feng Chen Feng Chen Qingmei Xie Qingmei Xie Qingmei Xie |
| author_sort | Wencheng Lin |
| collection | DOAJ |
| description | Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection, resulting in great economic losses. Although ALV-J-induced immunosuppression has been well established, the underlying molecular mechanism for such induction is still unclear. Here, we report that the inhibitory effect of ALV-J infection on type I interferon expression is associated with the down-regulation of transcriptional regulator NF-κB in host cells. We found that ALV-J possess the inhibitory effect on type I interferon production in HD11 cells and that ALV-J causes the up-regulation of IκBα and down-regulation of NF-κB p65, and that ALV-J blocks the phosphorylation of IκBα on Ser32/36 amino acid residues. Collectively, our findings provide insights into the pathogenesis of ALV-J. |
| first_indexed | 2024-12-12T08:29:53Z |
| format | Article |
| id | doaj.art-98f7781475c04fb1b6602df634c1afed |
| institution | Directory Open Access Journal |
| issn | 1664-302X |
| language | English |
| last_indexed | 2024-12-12T08:29:53Z |
| publishDate | 2018-05-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Microbiology |
| spelling | doaj.art-98f7781475c04fb1b6602df634c1afed2022-12-22T00:31:08ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2018-05-01910.3389/fmicb.2018.01089352377Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB PhosphorylationWencheng Lin0Wencheng Lin1Wencheng Lin2Zhouyi Xu3Yiming Yan4Huanmin Zhang5Hongxin Li6Hongxin Li7Hongxin Li8Weiguo Chen9Weiguo Chen10Weiguo Chen11Feng Chen12Feng Chen13Feng Chen14Qingmei Xie15Qingmei Xie16Qingmei Xie17Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, ChinaSouth China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, ChinaKey Laboratory of Animal Health Aquaculture and Environmental Control, Guangzhou, ChinaGuangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, ChinaGuangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, ChinaAvian Disease and Oncology Laboratory, USDA, Agriculture Research Service, East Lansing, MI, United StatesGuangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, ChinaSouth China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, ChinaKey Laboratory of Animal Health Aquaculture and Environmental Control, Guangzhou, ChinaGuangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, ChinaSouth China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, ChinaKey Laboratory of Animal Health Aquaculture and Environmental Control, Guangzhou, ChinaGuangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, ChinaSouth China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, ChinaKey Laboratory of Animal Health Aquaculture and Environmental Control, Guangzhou, ChinaGuangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, ChinaSouth China Collaborative Innovation Center for Poultry Disease Control and Product Safety, Guangzhou, ChinaKey Laboratory of Animal Health Aquaculture and Environmental Control, Guangzhou, ChinaAvian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection, resulting in great economic losses. Although ALV-J-induced immunosuppression has been well established, the underlying molecular mechanism for such induction is still unclear. Here, we report that the inhibitory effect of ALV-J infection on type I interferon expression is associated with the down-regulation of transcriptional regulator NF-κB in host cells. We found that ALV-J possess the inhibitory effect on type I interferon production in HD11 cells and that ALV-J causes the up-regulation of IκBα and down-regulation of NF-κB p65, and that ALV-J blocks the phosphorylation of IκBα on Ser32/36 amino acid residues. Collectively, our findings provide insights into the pathogenesis of ALV-J.https://www.frontiersin.org/article/10.3389/fmicb.2018.01089/fullALV-Jimmunosuppressionmacrophagetype I interferonNF-κB |
| spellingShingle | Wencheng Lin Wencheng Lin Wencheng Lin Zhouyi Xu Yiming Yan Huanmin Zhang Hongxin Li Hongxin Li Hongxin Li Weiguo Chen Weiguo Chen Weiguo Chen Feng Chen Feng Chen Feng Chen Qingmei Xie Qingmei Xie Qingmei Xie Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation Frontiers in Microbiology ALV-J immunosuppression macrophage type I interferon NF-κB |
| title | Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation |
| title_full | Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation |
| title_fullStr | Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation |
| title_full_unstemmed | Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation |
| title_short | Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation |
| title_sort | avian leukosis virus subgroup j attenuates type i interferon production through blocking iκb phosphorylation |
| topic | ALV-J immunosuppression macrophage type I interferon NF-κB |
| url | https://www.frontiersin.org/article/10.3389/fmicb.2018.01089/full |
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