دورية أكاديمية
APOBEC3-related mutations in the spike protein-encoding region facilitate SARS-CoV-2 evolution
| العنوان: | APOBEC3-related mutations in the spike protein-encoding region facilitate SARS-CoV-2 evolution |
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| المؤلفون: | Jiaying Shen, Xinxin Xu, Junyan Fan, Hongsen Chen, Yue Zhao, Weijin Huang, Wenbin Liu, Zihan Zhang, Qianqian Cui, Qianqian Li, Zheyun Niu, Dongming Jiang, Guangwen Cao |
| المصدر: | Heliyon, Vol 10, Iss 11, Pp e32139- (2024) |
| بيانات النشر: | Elsevier, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Science (General) LCC:Social sciences (General) |
| مصطلحات موضوعية: | COVID-19, SARS-CoV-2, APOBEC3, A3B, RNA editing, Inflammation, Science (General), Q1-390, Social sciences (General), H1-99 |
| الوصف: | SARS-CoV-2 evolves gradually to cause COVID-19 epidemic. One of driving forces of SARS-CoV-2 evolution might be activation of apolipoprotein B mRNA editing catalytic subunit-like protein 3 (APOBEC3) by inflammatory factors. Here, we aimed to elucidate the effect of the APOBEC3-related viral mutations on the infectivity and immune evasion of SARS-CoV-2. The APOBEC3-related C > U mutations ranked as the second most common mutation types in the SARS-CoV-2 genome. mRNA expression of APOBEC3A (A3A), APOBEC3B (A3B), and APOBEC3G (A3G) in peripheral blood cells increased with disease severity. A3B, a critical member of the APOBEC3 family, was significantly upregulated in both severe and moderate COVID-19 patients and positively associated with neutrophil proportion and COVID-19 severity. We identified USP18 protein, a key molecule centralizing the protein-protein interaction network of key APOBEC3 proteins. Furthermore, mRNA expression of USP18 was significantly correlated to ACE2 and TMPRSS2 expression in the tissue of upper airways. Knockdown of USP18 mRNA significantly decreased A3B expression. Ectopic expression of A3B gene increased SARS-CoV-2 infectivity. C > U mutations at S371F, S373L, and S375F significantly conferred with the immune escape of SARS-CoV-2. Thus, APOBEC3, whose expression are upregulated by inflammatory factors, might promote SARS-CoV-2 evolution and spread via upregulating USP18 level and facilitating the immune escape. A3B and USP18 might be therapeutic targets for interfering with SARS-CoV-2 evolution. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2405-8440 |
| Relation: | http://www.sciencedirect.com/science/article/pii/S2405844024081702; https://doaj.org/toc/2405-8440 |
| DOI: | 10.1016/j.heliyon.2024.e32139 |
| URL الوصول: | https://doaj.org/article/3533df9087c044b99ef9d8c22c1e3b77 |
| رقم الأكسشن: | edsdoj.3533df9087c044b99ef9d8c22c1e3b77 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 24058440 |
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| DOI: | 10.1016/j.heliyon.2024.e32139 |