Untargeted Lipidomics of Vesicular Stomatitis Virus-Infected Cells and Viral Particles.
Untargeted Lipidomics of Vesicular Stomatitis Virus-Infected Cells and Viral Particles.
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DOI：
10.3390/v14010003
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发表时间：
2021-12-21
期刊：
影响因子：
--
通讯作者：
Brindley MA
中科院分区：
文献类型：
--
作者：
Havranek KE;Reyes Ballista JM;Hines KM;Brindley MA
病毒的生命周期严重依赖于宿主脂质。包膜病毒进入需要病毒和细胞膜融合。一旦感染发生，病毒可能依赖宿主脂质进行复制和输出。在出芽过程中，包膜病毒从宿主膜上获得脂质双分子层。此外，宿主脂质代谢和信号传导经常被劫持以促进病毒复制。我们采用非靶向HILIC-IM-MS脂质组学方法，鉴定了在水疱性口炎病毒（VSV）感染期间显著改变的宿主脂质种类。许多甘油磷脂和鞘脂类被修饰，本体富集分析表明，脂质谱的改变改变了宿主膜的性质。溶血磷脂酰胆碱（LPC）在感染过程中被耗尽，而一些神经酰胺鞘脂在感染过程中被增加，LPC可以促进膜曲率并作为信号分子。神经酰胺和鞘磷脂也在病毒颗粒中富集，表明鞘脂代谢在VSV感染过程中很重要。
The viral lifecycle is critically dependent upon host lipids. Enveloped viral entry requires fusion between viral and cellular membranes. Once an infection has occurred, viruses may rely on host lipids for replication and egress. Upon exit, enveloped viruses derive their lipid bilayer from host membranes during the budding process. Furthermore, host lipid metabolism and signaling are often hijacked to facilitate viral replication. We employed an untargeted HILIC-IM-MS lipidomics approach and identified host lipid species that were significantly altered during vesicular stomatitis virus (VSV) infection. Many glycerophospholipid and sphingolipid species were modified, and ontological enrichment analysis suggested that the alterations to the lipid profile change host membrane properties. Lysophosphatidylcholine (LPC), which can contribute to membrane curvature and serve as a signaling molecule, was depleted during infection, while several ceramide sphingolipids were augmented during infection. Ceramide and sphingomyelin lipids were also enriched in viral particles, indicating that sphingolipid metabolism is important during VSV infection.
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影响因子：
3.7
作者：
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通讯作者：
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作者：
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Schnell, MJ
影响因子：
30.3
作者：
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影响因子：
6.7
作者：
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通讯作者：
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囊泡口腔炎病毒的细胞致病发生受M蛋白的PSAP基序以物种依赖性方式调节。
DOI：
10.3390/v4091605
发表时间：
2012-09
期刊：
Viruses
影响因子：
--
作者：
Irie T;Liu Y;Drolet BS;Carnero E;García-Sastre A;Harty RN
通讯作者：
Harty RN