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寨卡病毒在细胞培养模型中的感染反映了患者的转录组特征。

Zika virus infection in a cell culture model reflects the transcriptomic signatures in patients.

作者信息

Berglund Gillian, Lennon Claudia D, Badu Pheonah, Berglund J Andrew, Pager Cara T

机构信息

RNA Institute, College of Arts and Sciences, University at Albany-SUNY, Albany, NY 12222, USA.

Department of Biological Sciences, College of Arts and Sciences, University at Albany-SUNY, Albany, NY 12222, USA.

出版信息

bioRxiv. 2024 May 25:2024.05.25.595842. doi: 10.1101/2024.05.25.595842.

DOI:10.1101/2024.05.25.595842
PMID:38826459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11142252/
Abstract

Zika virus (ZIKV), a re-emerging flavivirus, is associated with devasting developmental and neurological disease outcomes particularly in infants infected . Towards understanding the molecular underpinnings of the unique ZIKV disease pathologies, numerous transcriptome-wide studies have been undertaken. Notably, these studies have overlooked the assimilation of RNA-seq analysis from ZIKV-infected patients with cell culture model systems. In this study we find that ZIKV-infection of human lung adenocarcinoma A549 cells, mirrored both the transcriptional and alternative splicing profiles from previously published RNA-seq data of peripheral blood mononuclear cells collected from pediatric patients during early acute, late acute, and convalescent phases of ZIKV infection. Our analyses show that ZIKV infection in cultured cells correlates with transcriptional changes in patients, while the overlap in alternative splicing profiles was not as extensive. Overall, our data indicate that cell culture model systems support dissection of select molecular changes detected in patients and establishes the groundwork for future studies elucidating the biological implications of alternative splicing during ZIKV infection.

摘要

寨卡病毒(ZIKV)是一种再度出现的黄病毒,与严重的发育和神经疾病后果相关,尤其是在受感染的婴儿中。为了了解寨卡病毒独特疾病病理的分子基础,已经开展了许多全转录组研究。值得注意的是,这些研究忽略了将来自寨卡病毒感染患者的RNA测序分析与细胞培养模型系统进行整合。在本研究中,我们发现人肺腺癌A549细胞感染寨卡病毒后,反映了先前发表的、在寨卡病毒感染的早期急性期、晚期急性期和恢复期从儿科患者收集的外周血单个核细胞的RNA测序数据中的转录和可变剪接谱。我们的分析表明,培养细胞中的寨卡病毒感染与患者的转录变化相关,而可变剪接谱的重叠并不那么广泛。总体而言,我们的数据表明,细胞培养模型系统有助于剖析在患者中检测到的特定分子变化,并为未来阐明寨卡病毒感染期间可变剪接的生物学意义的研究奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/3010bde63d49/nihpp-2024.05.25.595842v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/cb5a95a355b8/nihpp-2024.05.25.595842v1-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/f971a1cd31cd/nihpp-2024.05.25.595842v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/c3bf87543599/nihpp-2024.05.25.595842v1-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/3010bde63d49/nihpp-2024.05.25.595842v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/cb5a95a355b8/nihpp-2024.05.25.595842v1-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/f971a1cd31cd/nihpp-2024.05.25.595842v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/c3bf87543599/nihpp-2024.05.25.595842v1-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7fc/11142252/3010bde63d49/nihpp-2024.05.25.595842v1-f0004.jpg

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2
UMP-CMP kinase 2 inhibits ZIKV replication through activation of type I IFN signaling pathway.UMP-CMP 激酶 2 通过激活 I 型 IFN 信号通路抑制 ZIKV 复制。
J Med Virol. 2024 Mar;96(3):e29533. doi: 10.1002/jmv.29533.
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HERC5-catalyzed ISGylation potentiates cGAS-mediated innate immunity.
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Cell Rep. 2024 Mar 26;43(3):113870. doi: 10.1016/j.celrep.2024.113870. Epub 2024 Feb 28.
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iScience. 2024 Jan 9;27(2):108820. doi: 10.1016/j.isci.2024.108820. eCollection 2024 Feb 16.
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The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses.激活转录因子 3(ATF3)在炎症、细胞凋亡、铁死亡和病原体感染反应中的双重作用。
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