Lipid metabolism is a novel and practical source of potential targets for antiviral discovery against porcine parvovirus

文献类型： 外文期刊

第一作者： Zhao, Zhanzhong

作者： Zhao, Zhanzhong;Li, Jing;Feng, Xiaohui;Tang, Xiangfang;Guo, Xiaoyu;Meng, Qingshi;Rao, Zhenghua;Zhang, Hongfu;Zhao, Xinghui;Feng, Li

作者机构：

关键词： Porcine parvovirus; Lipid metabolism; Cellular microenvironment; Propagation; Potential targets

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

ISSN： 0378-1135

年卷期： 2021 年 261 卷

页码：

收录情况： SCI

摘要： How parvovirus manipulates host lipid metabolism to facilitate its propagation, pathogenicity and consequences for disease, is poorly characterized. Here, we addressed this question using porcine parvovirus (PPV) to understand the complex interactions of parvovirus with lipid metabolism networks contributing to the identification of novel and practical antiviral candidates. PPV significantly alters host lipid composition, characteristic of subclasses of phospholipids and sphingolipids, and induces lipid droplets (LDs) formation via regulating calcium-independent PLA2 beta (iPLA2 beta), phospholipase C gamma 2 (PLC gamma 2), diacylglycerol kinase alpha (DKG alpha), phosphoinositide 3-kinase (PI3K), lysophosphatidic acid acyltransferase theta (LPAAT theta), and sphingosine kinases (SphK1 and SphK2). PPV utilizes and exploits these enzymes as well as their metabolites and host factors including MAPKs (p38 and ERK1/2), protein kinase C (PKC) and Ca2+ to induce S phase arrest, apoptosis and incomplete autophagy, all benefit to PPV propagation. PPV also suppresses prostaglandin E2 (PGE2) synthesis via downregulating cyclooxygenase-1 (COX-1), indicating PPV hijacks COX-1-PGE2 axis to evade immune surveillance. Our data support a model where PPV to establishes an optimal environment for its propagation and pathogenicity via co-opting host lipid metabolism, being positioned as a source of potential targets.

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