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昆金病毒、寨卡病毒和黄热病病毒感染对脑源性 U87 细胞的编码转录组和蛋白质组有不同的影响。

Kunjin Virus, Zika Virus, and Yellow Fever Virus Infections Have Distinct Effects on the Coding Transcriptome and Proteome of Brain-Derived U87 Cells.

机构信息

Département de Biochimie et de Génomique Fonctionnelle, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, 3201 rue Jean-Mignault, Sherbrooke, QC J1E 4K8, Canada.

Department of Microbiology, Immunology, and Pathology, School of Biomedical Engineering, Colorado State University, 1682 Campus Delivery, Fort Collins, CO 80523, USA.

出版信息

Viruses. 2023 Jun 23;15(7):1419. doi: 10.3390/v15071419.

DOI:10.3390/v15071419
PMID:37515107
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10385720/
Abstract

As obligate intracellular parasites, viruses rely heavily on host cells for replication, and therefore dysregulate several cellular processes for their benefit. In return, host cells activate multiple signaling pathways to limit viral replication and eradicate viruses. The present study explores the complex interplay between viruses and host cells through next generation RNA sequencing as well as mass spectrometry (SILAC). Both the coding transcriptome and the proteome of human brain-derived U87 cells infected with Kunjin virus, Zika virus, or Yellow Fever virus were compared to the transcriptome and the proteome of mock-infected cells. Changes in the abundance of several hundred mRNAs and proteins were found in each infection. Moreover, the alternative splicing of hundreds of mRNAs was found to be modulated upon viral infection. Interestingly, a significant disconnect between the changes in the transcriptome and those in the proteome of infected cells was observed. These findings provide a global view of the coding transcriptome and the proteome of Flavivirus-infected cells, leading to a better comprehension of Flavivirus-host interactions.

摘要

作为专性细胞内寄生虫,病毒严重依赖宿主细胞进行复制,因此会扰乱几种细胞过程以谋取自身利益。作为回报,宿主细胞会激活多种信号通路来限制病毒复制并消灭病毒。本研究通过下一代 RNA 测序和质谱(SILAC)技术探索了病毒和宿主细胞之间的复杂相互作用。比较了感染 Kunjin 病毒、寨卡病毒或黄热病病毒的人脑源性 U87 细胞的编码转录组和蛋白质组与mock 感染细胞的转录组和蛋白质组。在每种感染中都发现了数百个 mRNA 和蛋白质丰度的变化。此外,还发现数百个 mRNA 的可变剪接在病毒感染时被调节。有趣的是,观察到感染细胞的转录组和蛋白质组的变化之间存在显著脱节。这些发现提供了 Flavivirus 感染细胞的编码转录组和蛋白质组的全面视图,有助于更好地理解 Flavivirus-宿主相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/755b6e8afdb3/viruses-15-01419-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/81543487de50/viruses-15-01419-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/a90c2267e91c/viruses-15-01419-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/34d5f4d44ecb/viruses-15-01419-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/4906df5a8f07/viruses-15-01419-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/87c97fd91c85/viruses-15-01419-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/941f9dbf3b70/viruses-15-01419-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/5170376c03d1/viruses-15-01419-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/755b6e8afdb3/viruses-15-01419-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/81543487de50/viruses-15-01419-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/a90c2267e91c/viruses-15-01419-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/34d5f4d44ecb/viruses-15-01419-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/4906df5a8f07/viruses-15-01419-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/87c97fd91c85/viruses-15-01419-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/941f9dbf3b70/viruses-15-01419-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/5170376c03d1/viruses-15-01419-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95d/10385720/755b6e8afdb3/viruses-15-01419-g008.jpg

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