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在原代细胞的从头裂解性感染过程中,γ疱疹病毒 DNA 与核心组蛋白的动态关联。

Dynamic association of gammaherpesvirus DNA with core histone during de novo lytic infection of primary cells.

机构信息

Department of Microbiology and Molecular Genetics, Cancer Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

出版信息

Virology. 2011 Dec 20;421(2):167-72. doi: 10.1016/j.virol.2011.09.024. Epub 2011 Oct 20.

DOI:10.1016/j.virol.2011.09.024
PMID:22018782
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3210866/
Abstract

Association of herpesvirus DNA with histones has important implications for lytic and latent infections; thus herpesviruses arbitrate interactions with histones to productively infect host cells. While regulation of alpha and betaherpesvirus chromatin during lytic infection has been actively investigated, very little is known about interaction of gammaherpesvirus DNA with histones upon de novo lytic infection. Murine gammaherpesvirus-68 (MHV68) is a rodent pathogen that offers a tractable system to study gammaherpesvirus lytic infection in primary cells. In this study we report that MHV68 promoter and orilyt sequences underwent dynamic association with histone H3 during de novo lytic infection of primary macrophages and fibroblasts. Similar to HSV-1, the degree of MHV68 DNA association with histone H3 was dependent on the multiplicity of infection and was further regulated by viral DNA synthesis. Our work sets a precedent for future studies of gammaherpesvirus chromatin during de novo lytic infection.

摘要

疱疹病毒 DNA 与组蛋白的关联对裂解和潜伏感染具有重要意义;因此,疱疹病毒通过与组蛋白的相互作用来有效地感染宿主细胞。虽然在裂解感染过程中已经积极研究了α和β疱疹病毒染色质的调控,但对于新出现的裂解感染时γ疱疹病毒 DNA 与组蛋白的相互作用知之甚少。鼠γ疱疹病毒-68(MHV68)是一种啮齿动物病原体,为研究原发性细胞中的γ疱疹病毒裂解感染提供了一个易于处理的系统。在这项研究中,我们报告说,在原代巨噬细胞和成纤维细胞的新出现的裂解感染过程中,MHV68 启动子和 ORF 序列与组蛋白 H3 发生动态关联。与 HSV-1 相似,MHV68 DNA 与组蛋白 H3 的关联程度取决于感染复数,并进一步受到病毒 DNA 合成的调节。我们的工作为未来研究新出现的裂解感染过程中的γ疱疹病毒染色质奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9afc/3210866/89728ac8d6d9/nihms328967f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9afc/3210866/05346d167385/nihms328967f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9afc/3210866/9fe52d4538be/nihms328967f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9afc/3210866/89728ac8d6d9/nihms328967f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9afc/3210866/05346d167385/nihms328967f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9afc/3210866/9fe52d4538be/nihms328967f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9afc/3210866/89728ac8d6d9/nihms328967f3.jpg

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本文引用的文献

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PLoS Pathog. 2010 Jun 3;6(6):e1000935. doi: 10.1371/journal.ppat.1000935.
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Transcriptional coactivator HCF-1 couples the histone chaperone Asf1b to HSV-1 DNA replication components.转录共激活因子 HCF-1 将组蛋白伴侣 Asf1b 与 HSV-1 DNA 复制成分偶联。
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Gammaherpesvirus-driven plasma cell differentiation regulates virus reactivation from latently infected B lymphocytes.
IFN-γ 抑制巨噬细胞中鼠疱疹病毒-68 的复制作用被 SOCS1 表达的诱导所拮抗。
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Liver X Receptors Suppress Activity of Cholesterol and Fatty Acid Synthesis Pathways To Oppose Gammaherpesvirus Replication.肝 X 受体抑制胆固醇和脂肪酸合成途径的活性以抵抗γ疱疹病毒复制。
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B Cell-Specific Expression of Ataxia-Telangiectasia Mutated Protein Kinase Promotes Chronic Gammaherpesvirus Infection.共济失调毛细血管扩张症突变蛋白激酶在B细胞中的特异性表达促进慢性γ疱疹病毒感染。
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