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通过激活肝脏X受体抑制人巨细胞病毒颗粒成熟

Inhibition of Human Cytomegalovirus Particle Maturation by Activation of Liver X Receptor.

作者信息

Liu Bingnan, Ma Yanping, Huang Yujing, Liu Zhongyang, Ruan Qiang, Qi Ying

机构信息

Virology Laboratory, Shengjing Hospital of China Medical University, Shenyang, China.

Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.

出版信息

Front Microbiol. 2022 Mar 7;13:846386. doi: 10.3389/fmicb.2022.846386. eCollection 2022.

DOI:10.3389/fmicb.2022.846386
PMID:35330771
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8940258/
Abstract

Human cytomegalovirus (HCMV), a herpesvirus family member, is a large, complex enveloped virus. The activation of liver X receptor (LXR) can significantly inhibit the replication of HCMV and weaken the virulence of progeny virus (unpublished data). Our results showed activated LXR affected some important viral protein expression and reduced cholesterol content in HCMV infected cells and virus particles. To further clarify the influence of activated LXR on HCMV replication, HCMV assembly and maturation processes were studied by transmission electron microscopy (TEM) in HCMV infected foreskin fibroblasts treated with LXR agonist GW3965. Results showed that activated LXR could reduce the envelope integrity of maturating virions. The functional stage of activated LXR on viral envelope integrity was mainly at virus assembly compartment (VAC) mediated envelopment but not structurally complete virus nucleocapsid formation and the egress of nucleocapsid from the nucleus to the cytoplasm mediated by nuclear egress complex. Reduced cholesterol synthesis and viral protein expression might interfere with the VAC-mediated envelopment. The nucleocapsid and tegument proteins enter the VAC area for the secondary envelope, which was interfered with and resulted in the defective particle, thereby affecting the amount and infectivity of the mature virus. The results indicate that inhibition of HCMV maturation is one mechanism of activated LXR inhibiting virus replication in infected cells.

摘要

人巨细胞病毒（HCMV）是疱疹病毒家族成员，是一种大型复杂的包膜病毒。肝X受体（LXR）的激活可显著抑制HCMV的复制并减弱子代病毒的毒力（未发表数据）。我们的结果表明，激活的LXR影响了一些重要病毒蛋白的表达，并降低了HCMV感染细胞和病毒颗粒中的胆固醇含量。为了进一步阐明激活的LXR对HCMV复制的影响，我们在用LXR激动剂GW3965处理的HCMV感染的包皮成纤维细胞中，通过透射电子显微镜（TEM）研究了HCMV的组装和成熟过程。结果表明，激活的LXR可降低成熟病毒粒子的包膜完整性。激活的LXR对病毒包膜完整性的作用阶段主要在病毒组装区室（VAC）介导的包膜形成过程中，而不是在结构完整的病毒核衣壳形成以及由核输出复合物介导的核衣壳从细胞核到细胞质的输出过程中。胆固醇合成减少和病毒蛋白表达降低可能会干扰VAC介导的包膜形成。核衣壳和衣壳蛋白进入VAC区域进行二次包膜形成，这一过程受到干扰并导致缺陷颗粒的产生，从而影响成熟病毒的数量和感染性。结果表明抑制HCMV成熟是激活的LXR抑制感染细胞中病毒复制的一种机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/65c22bd08db0/fmicb-13-846386-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/bc148762188d/fmicb-13-846386-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/63e1f0525c40/fmicb-13-846386-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/35c9430633fc/fmicb-13-846386-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/3c212d03a984/fmicb-13-846386-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/65c22bd08db0/fmicb-13-846386-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/bc148762188d/fmicb-13-846386-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/63e1f0525c40/fmicb-13-846386-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/35c9430633fc/fmicb-13-846386-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/3c212d03a984/fmicb-13-846386-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be9/8940258/65c22bd08db0/fmicb-13-846386-g005.jpg

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