دورية أكاديمية

Human coronaviruses disassemble processing bodies.

التفاصيل البيبلوغرافية
العنوان: Human coronaviruses disassemble processing bodies.
المؤلفون: Mariel Kleer, Rory P Mulloy, Carolyn-Ann Robinson, Danyel Evseev, Maxwell P Bui-Marinos, Elizabeth L Castle, Arinjay Banerjee, Samira Mubareka, Karen Mossman, Jennifer A Corcoran
المصدر: PLoS Pathogens, Vol 18, Iss 8, p e1010724 (2022)
بيانات النشر: Public Library of Science (PLoS), 2022.
سنة النشر: 2022
المجموعة: LCC:Immunologic diseases. Allergy
LCC:Biology (General)
مصطلحات موضوعية: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
الوصف: A dysregulated proinflammatory cytokine response is characteristic of severe coronavirus infections caused by SARS-CoV-2, yet our understanding of the underlying mechanism responsible for this imbalanced immune response remains incomplete. Processing bodies (PBs) are cytoplasmic membraneless ribonucleoprotein granules that control innate immune responses by mediating the constitutive decay or suppression of mRNA transcripts, including many that encode proinflammatory cytokines. PB formation promotes turnover or suppression of cytokine RNAs, whereas PB disassembly corresponds with the increased stability and/or translation of these cytokine RNAs. Many viruses cause PB disassembly, an event that can be viewed as a switch that rapidly relieves cytokine RNA repression and permits the infected cell to respond to viral infection. Prior to this submission, no information was known about how human coronaviruses (CoVs) impacted PBs. Here, we show SARS-CoV-2 and the common cold CoVs, OC43 and 229E, induced PB loss. We screened a SARS-CoV-2 gene library and identified that expression of the viral nucleocapsid (N) protein from SARS-CoV-2 was sufficient to mediate PB disassembly. RNA fluorescent in situ hybridization revealed that transcripts encoding TNF and IL-6 localized to PBs in control cells. PB loss correlated with the increased cytoplasmic localization of these transcripts in SARS-CoV-2 N protein-expressing cells. Ectopic expression of the N proteins from five other human coronaviruses (OC43, MERS, 229E, NL63 and SARS-CoV) did not cause significant PB disassembly, suggesting that this feature is unique to SARS-CoV-2 N protein. These data suggest that SARS-CoV-2-mediated PB disassembly contributes to the dysregulation of proinflammatory cytokine production observed during severe SARS-CoV-2 infection.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1553-7366
1553-7374
Relation: https://doaj.org/toc/1553-7366; https://doaj.org/toc/1553-7374
DOI: 10.1371/journal.ppat.1010724
URL الوصول: https://doaj.org/article/d838142f9f9f4db2a5a287c019f8e52e
رقم الأكسشن: edsdoj.838142f9f9f4db2a5a287c019f8e52e
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:15537366
15537374
DOI:10.1371/journal.ppat.1010724