CD59 association with infectious bronchitis virus particles protects against antibody-dependent complement-mediated lysis
| Autor: | Kangyu Li, Chang Yanyan, Dan Yan, Yun Zhang, Huichen Guo, Yanhong Ji, Ding Xiang Liu, Xiaoying Zhi, Shi-Chong Han, Gao Yuan, Yanquan Wei, Shiqi Sun |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
animal structures Lysis Short Communication Infectious bronchitis virus CD59 Antigens chemical and pharmacologic phenomena CD59 medicine.disease_cause Cleavage (embryo) Antibodies Cell Line Microbiology 03 medical and health sciences 0302 clinical medicine Virology medicine Animals Humans Immunologic Factors Immune Evasion Coronavirus Gene knockdown biology Complement System Proteins Complement system 030104 developmental biology Host-Pathogen Interactions embryonic structures biology.protein Antibody Protein Binding 030215 immunology |
| Zdroj: | Journal of General Virology |
| ISSN: | 1465-2099 0022-1317 |
| DOI: | 10.1099/jgv.0.000962 |
| Popis: | CD59 protein functions as a negative regulator of the terminal pathway of the complement system by binding to the C8/C9 factors. To date, little is known about the role of CD59 in coronavirus infectious bronchitis virus (IBV) infection. In this study, we discovered that CD59 was downregulated in IBV-infected cells and was associated with IBV virions. This association protected IBV particles from antibody-dependent complement-mediated lysis. IBV titres in the supernatant were significantly increased when CD59 proteins were overexpressed in cells followed by IBV infection, and this observation was further supported by knockdown or cleavage of CD59. Because no considerable change in IBV N protein and viral RNA levels was detected in total cell lysates prepared from the overexpression, knockdown or cleavage of CD59 groups, our data indicated that CD59 was involved in IBV particle release and that IBV had evolved a mechanism to utilize CD59 to evade complement-mediated destruction. |
| Databáze: | OpenAIRE |
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