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代谢组学分析揭示了4型禽腺病毒感染的新见解。

Metabolomic Profiling Reveals New Insight of Fowl Adenovirus Serotype 4 Infection.

作者信息

Ma Haiying, Niu Yujuan

机构信息

The Biomedical Sciences Institute of Qingdao University (Qingdao Branch of SJTU Bio-X Institutes), Qingdao University, Qingdao, China.

出版信息

Front Microbiol. 2022 Jan 17;12:784745. doi: 10.3389/fmicb.2021.784745. eCollection 2021.

DOI:10.3389/fmicb.2021.784745
PMID:35111140
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8801735/
Abstract

Highly pathogenic fowl adenovirus serotype 4 (FAdV-4) is the causative agent of hydropericardium syndrome (HPS), which is characterized by pericardial effusion and hepatitis, and is one of the foremost causes of economic losses to the poultry industry over the last 30 years. However, the metabolic changes in cells in response to FAdV-4 infection remain unclear. In order to understand the metabolic interactions between the host cell and virus, we utilized ultra-high-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry to analyze the metabolic profiles with hepatocellular carcinoma cell line (LMH) infected with FAdV-4. The results showed that FAdV-4 could restore metabolic networks in LMH cells and tricarboxylic acid cycle, glycolysis, and metabolism of purines, pyrimidines, alanine, aspartate, glutamate, and amino sugar and nucleotide sugar moieties. Moreover, FAdV-4 production was significantly reduced in LMH cells cultured in glucose or glutamine-deficient medium. These observations highlighted the importance of host cell metabolism in virus replication. Therefore, similarities and disparities in FAdV-4-regulation of the metabolism of host cells could help improve targeted drug and reduce infection.

摘要

高致病性禽腺病毒4型（FAdV-4）是心包积水综合征（HPS）的病原体，其特征为心包积液和肝炎，是过去30年家禽业经济损失的主要原因之一。然而，细胞对FAdV-4感染的代谢变化仍不清楚。为了了解宿主细胞与病毒之间的代谢相互作用，我们利用超高效液相色谱/四极杆飞行时间串联质谱分析感染FAdV-4的肝癌细胞系（LMH）的代谢谱。结果表明，FAdV-4可恢复LMH细胞中的代谢网络以及三羧酸循环、糖酵解，嘌呤、嘧啶、丙氨酸、天冬氨酸、谷氨酸以及氨基糖和核苷酸糖部分的代谢。此外，在葡萄糖或谷氨酰胺缺乏的培养基中培养的LMH细胞中，FAdV-4的产生显著减少。这些观察结果突出了宿主细胞代谢在病毒复制中的重要性。因此，FAdV-4对宿主细胞代谢调节的异同有助于改进靶向药物并减少感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/7f913dd028b8/fmicb-12-784745-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/4f1f240a7a21/fmicb-12-784745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/9dcbc4d5ded1/fmicb-12-784745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/23ca4795b3ca/fmicb-12-784745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/1879c670fbbc/fmicb-12-784745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/e7f83da29284/fmicb-12-784745-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/f8bfe4e68e63/fmicb-12-784745-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/039713b6a081/fmicb-12-784745-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/7f913dd028b8/fmicb-12-784745-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/4f1f240a7a21/fmicb-12-784745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/9dcbc4d5ded1/fmicb-12-784745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/23ca4795b3ca/fmicb-12-784745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/1879c670fbbc/fmicb-12-784745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/e7f83da29284/fmicb-12-784745-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/f8bfe4e68e63/fmicb-12-784745-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/039713b6a081/fmicb-12-784745-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3674/8801735/7f913dd028b8/fmicb-12-784745-g008.jpg

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