دورية أكاديمية

Pseudorabies virus VHS protein abrogates interferon responses by blocking NF-κB and IRF3 nuclear translocation.

التفاصيل البيبلوغرافية
العنوان: Pseudorabies virus VHS protein abrogates interferon responses by blocking NF-κB and IRF3 nuclear translocation.
المؤلفون: Yan Z; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China., Yue J; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China., Zhang Y; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China., Hou Z; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China., Li D; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China., Yang Y; College of Life Science and Engineering, Northwest Minzu University, Lanzhou, 730030, China., Li X; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China; Gansu Tech Innovation Center of Animal Cell, Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China; Engineering Research Center of Key Technology and Industrialization of Cell-based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China., Idris A; Centre for Immunology and Infection Control, School of Biomedical Sciences, Queensland University of Technology, Kelvin Grove, Queensland, 4702, Australia., Li H; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China., Li S; College of Life Science and Engineering, Northwest Minzu University, Lanzhou, 730030, China., Xie J; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China; College of Life Science and Engineering, Northwest Minzu University, Lanzhou, 730030, China. Electronic address: xjy_1314@126.com., Feng R; Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China; Gansu Tech Innovation Center of Animal Cell, Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China; Engineering Research Center of Key Technology and Industrialization of Cell-based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China. Electronic address: fengruofei@xbmu.edu.cn.
المصدر: Virologica Sinica [Virol Sin] 2024 Aug; Vol. 39 (4), pp. 587-599. Date of Electronic Publication: 2024 May 30.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier B.V. on behalf of KeAi Communications Co. Ltd Country of Publication: Netherlands NLM ID: 101514185 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1995-820X (Electronic) Linking ISSN: 1995820X NLM ISO Abbreviation: Virol Sin Subsets: MEDLINE
أسماء مطبوعة: Publication: 2022- : [Amsterdam, Netherlands] : Elsevier B.V. on behalf of KeAi Communications Co. Ltd.
Original Publication: Beijing : Science Press
مواضيع طبية MeSH: Herpesvirus 1, Suid*/immunology , Herpesvirus 1, Suid*/genetics , Interferon Regulatory Factor-3*/metabolism , Interferon Regulatory Factor-3*/genetics , Immune Evasion* , NF-kappa B*/metabolism , NF-kappa B*/genetics , NF-kappa B*/immunology, Animals ; Swine ; Humans ; Interferons/immunology ; Interferons/metabolism ; Interferons/genetics ; Pseudorabies/virology ; Pseudorabies/immunology ; Cell Line ; Host-Pathogen Interactions/immunology ; Viral Proteins/genetics ; Viral Proteins/metabolism ; Viral Proteins/immunology ; HEK293 Cells ; Phosphorylation ; Protein Transport
مستخلص: Herpesviruses antagonize host antiviral responses through a myriad of molecular strategies culminating in the death of the host cells. Pseudorabies virus (PRV) is a significant veterinary pathogen in pigs, causing neurological sequalae that ultimately lead to the animal's demise. PRV is known to trigger apoptotic cell death during the late stages of infection. The virion host shutdown protein (VHS) encoded by UL41 plays a crucial role in the PRV infection process. In this study, we demonstrate that UL41 inhibits PRV-induced activation of inflammatory cytokine and negatively regulates the cGAS-STING-mediated antiviral activity by targeting IRF3, thereby inhibiting the translocation and phosphorylation of IRF3. Notably, mutating the conserved amino acid sites (E192, D194, and D195) in the RNase domain of UL41 or knocking down UL41 inhibits the immune evasion of PRV, suggesting that UL41 may play a crucial role in PRV's evasion of the host immune response during infection. These results enhance our understanding of how PRV structural proteins assist the virus in evading the host immune response.
Competing Interests: Conflict of interest All authors declare that there are no competing interests.
(Copyright © 2024 The Authors. Publishing services by Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: IRF3; Interferon; Pseudorabies virus (PRV); UL41; cGAS-STING
المشرفين على المادة: 0 (Interferon Regulatory Factor-3)
0 (NF-kappa B)
9008-11-1 (Interferons)
0 (Viral Proteins)
تواريخ الأحداث: Date Created: 20240601 Date Completed: 20240823 Latest Revision: 20240827
رمز التحديث: 20240828
DOI: 10.1016/j.virs.2024.05.009
PMID: 38823782
قاعدة البيانات: MEDLINE
الوصف
تدمد:1995-820X
DOI:10.1016/j.virs.2024.05.009