Phosphatidic acid phosphatase 1 impairs SARS-CoV-2 replication by affecting the glycerophospholipid metabolism pathway
Viruses exploit the host lipid metabolism machinery to achieve efficient replication. We herein characterize the lipids profile reprogramming in vitro and in vivo using liquid chromatography-mass spectrometry-based untargeted lipidomics. The lipidome of SARS-CoV-2-infected Caco-2 cells was markedly...
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| Veröffentlicht in: | International journal of biological sciences 2022-01, Vol.18 (12), p.4744-4755 |
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| creator | Yan, Bingpeng Yuan, Shuofeng Cao, Jianli Fung, Kingchun Lai, Pok-Man Yin, Feifei Sze, Kong-Hung Qin, Zhenzhi Xie, Yubin Ye, Zi-Wei Yuen, Terrence Tsz-Tai Chik, Kenn Ka-Heng Tsang, Jessica Oi-Ling Zou, Zijiao Chan, Chris Chun-Yiu Luo, Cuiting Cai, Jian-Piao Chan, Kwok-Hung Chung, Tom Wai-Hing Tam, Anthony Raymond Chu, Hin Jin, Dong-Yan Hung, Ivan Fan-Ngai Yuen, Kwok-Yung Kao, Richard Yi-Tsun Chan, Jasper Fuk-Woo |
| description | Viruses exploit the host lipid metabolism machinery to achieve efficient replication. We herein characterize the lipids profile reprogramming in vitro and in vivo using liquid chromatography-mass spectrometry-based untargeted lipidomics. The lipidome of SARS-CoV-2-infected Caco-2 cells was markedly different from that of mock-infected samples, with most of the changes involving downregulation of ceramides. In COVID-19 patients' plasma samples, a total of 54 lipids belonging to 12 lipid classes that were significantly perturbed compared to non-infected control subjects' plasma samples were identified. Among these 12 lipid classes, ether-linked phosphatidylcholines, ether-linked phosphatidylethanolamines, phosphatidylcholines, and ceramides were the four most perturbed. Pathway analysis revealed that the glycerophospholipid, sphingolipid, and ether lipid metabolisms pathway were the most significantly perturbed host pathways. Phosphatidic acid phosphatases (PAP) were involved in all three pathways and PAP-1 deficiency significantly suppressed SARS-CoV-2 replication. siRNA knockdown of LPIN2 and LPIN3 resulted in significant reduction of SARS-CoV-2 load. In summary, these findings characterized the host lipidomic changes upon SARS-CoV-2 infection and identified PAP-1 as a potential target for intervention for COVID-19. |
| doi_str_mv | 10.7150/ijbs.73057 |
| format | Article |
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We herein characterize the lipids profile reprogramming in vitro and in vivo using liquid chromatography-mass spectrometry-based untargeted lipidomics. The lipidome of SARS-CoV-2-infected Caco-2 cells was markedly different from that of mock-infected samples, with most of the changes involving downregulation of ceramides. In COVID-19 patients' plasma samples, a total of 54 lipids belonging to 12 lipid classes that were significantly perturbed compared to non-infected control subjects' plasma samples were identified. Among these 12 lipid classes, ether-linked phosphatidylcholines, ether-linked phosphatidylethanolamines, phosphatidylcholines, and ceramides were the four most perturbed. Pathway analysis revealed that the glycerophospholipid, sphingolipid, and ether lipid metabolisms pathway were the most significantly perturbed host pathways. Phosphatidic acid phosphatases (PAP) were involved in all three pathways and PAP-1 deficiency significantly suppressed SARS-CoV-2 replication. siRNA knockdown of LPIN2 and LPIN3 resulted in significant reduction of SARS-CoV-2 load. In summary, these findings characterized the host lipidomic changes upon SARS-CoV-2 infection and identified PAP-1 as a potential target for intervention for COVID-19.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.73057</identifier><identifier>PMID: 35874954</identifier><language>eng</language><publisher>Sydney: Ivyspring International Publisher Pty Ltd</publisher><subject>Acid phosphatase ; Coronaviruses ; COVID-19 ; Lipid metabolism ; Lipids ; Liquid chromatography ; Mass spectrometry ; Mass spectroscopy ; Phosphatidic acid ; Phosphatidylethanolamine ; Replication ; Research Paper ; Severe acute respiratory syndrome coronavirus 2 ; siRNA ; Viral diseases ; Viruses</subject><ispartof>International journal of biological sciences, 2022-01, Vol.18 (12), p.4744-4755</ispartof><rights>2022. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c383t-1b74d9a9b37b0ebe27277ae23ae56574db37d88ca03c331c39ae809c81e6f6853</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9305268/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9305268/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids></links><search><creatorcontrib>Yan, Bingpeng</creatorcontrib><creatorcontrib>Yuan, Shuofeng</creatorcontrib><creatorcontrib>Cao, Jianli</creatorcontrib><creatorcontrib>Fung, Kingchun</creatorcontrib><creatorcontrib>Lai, Pok-Man</creatorcontrib><creatorcontrib>Yin, Feifei</creatorcontrib><creatorcontrib>Sze, Kong-Hung</creatorcontrib><creatorcontrib>Qin, Zhenzhi</creatorcontrib><creatorcontrib>Xie, Yubin</creatorcontrib><creatorcontrib>Ye, Zi-Wei</creatorcontrib><creatorcontrib>Yuen, Terrence Tsz-Tai</creatorcontrib><creatorcontrib>Chik, Kenn Ka-Heng</creatorcontrib><creatorcontrib>Tsang, Jessica Oi-Ling</creatorcontrib><creatorcontrib>Zou, Zijiao</creatorcontrib><creatorcontrib>Chan, Chris Chun-Yiu</creatorcontrib><creatorcontrib>Luo, Cuiting</creatorcontrib><creatorcontrib>Cai, Jian-Piao</creatorcontrib><creatorcontrib>Chan, Kwok-Hung</creatorcontrib><creatorcontrib>Chung, Tom Wai-Hing</creatorcontrib><creatorcontrib>Tam, Anthony Raymond</creatorcontrib><creatorcontrib>Chu, Hin</creatorcontrib><creatorcontrib>Jin, Dong-Yan</creatorcontrib><creatorcontrib>Hung, Ivan Fan-Ngai</creatorcontrib><creatorcontrib>Yuen, Kwok-Yung</creatorcontrib><creatorcontrib>Kao, Richard Yi-Tsun</creatorcontrib><creatorcontrib>Chan, Jasper Fuk-Woo</creatorcontrib><title>Phosphatidic acid phosphatase 1 impairs SARS-CoV-2 replication by affecting the glycerophospholipid metabolism pathway</title><title>International journal of biological sciences</title><description>Viruses exploit the host lipid metabolism machinery to achieve efficient replication. We herein characterize the lipids profile reprogramming in vitro and in vivo using liquid chromatography-mass spectrometry-based untargeted lipidomics. The lipidome of SARS-CoV-2-infected Caco-2 cells was markedly different from that of mock-infected samples, with most of the changes involving downregulation of ceramides. In COVID-19 patients' plasma samples, a total of 54 lipids belonging to 12 lipid classes that were significantly perturbed compared to non-infected control subjects' plasma samples were identified. Among these 12 lipid classes, ether-linked phosphatidylcholines, ether-linked phosphatidylethanolamines, phosphatidylcholines, and ceramides were the four most perturbed. Pathway analysis revealed that the glycerophospholipid, sphingolipid, and ether lipid metabolisms pathway were the most significantly perturbed host pathways. Phosphatidic acid phosphatases (PAP) were involved in all three pathways and PAP-1 deficiency significantly suppressed SARS-CoV-2 replication. siRNA knockdown of LPIN2 and LPIN3 resulted in significant reduction of SARS-CoV-2 load. In summary, these findings characterized the host lipidomic changes upon SARS-CoV-2 infection and identified PAP-1 as a potential target for intervention for COVID-19.</description><subject>Acid phosphatase</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Liquid chromatography</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Phosphatidic acid</subject><subject>Phosphatidylethanolamine</subject><subject>Replication</subject><subject>Research Paper</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>siRNA</subject><subject>Viral 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Pok-Man</au><au>Yin, Feifei</au><au>Sze, Kong-Hung</au><au>Qin, Zhenzhi</au><au>Xie, Yubin</au><au>Ye, Zi-Wei</au><au>Yuen, Terrence Tsz-Tai</au><au>Chik, Kenn Ka-Heng</au><au>Tsang, Jessica Oi-Ling</au><au>Zou, Zijiao</au><au>Chan, Chris Chun-Yiu</au><au>Luo, Cuiting</au><au>Cai, Jian-Piao</au><au>Chan, Kwok-Hung</au><au>Chung, Tom Wai-Hing</au><au>Tam, Anthony Raymond</au><au>Chu, Hin</au><au>Jin, Dong-Yan</au><au>Hung, Ivan Fan-Ngai</au><au>Yuen, Kwok-Yung</au><au>Kao, Richard Yi-Tsun</au><au>Chan, Jasper Fuk-Woo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Phosphatidic acid phosphatase 1 impairs SARS-CoV-2 replication by affecting the glycerophospholipid metabolism pathway</atitle><jtitle>International journal of biological sciences</jtitle><date>2022-01-01</date><risdate>2022</risdate><volume>18</volume><issue>12</issue><spage>4744</spage><epage>4755</epage><pages>4744-4755</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>Viruses exploit the host lipid metabolism machinery to achieve efficient replication. We herein characterize the lipids profile reprogramming in vitro and in vivo using liquid chromatography-mass spectrometry-based untargeted lipidomics. The lipidome of SARS-CoV-2-infected Caco-2 cells was markedly different from that of mock-infected samples, with most of the changes involving downregulation of ceramides. In COVID-19 patients' plasma samples, a total of 54 lipids belonging to 12 lipid classes that were significantly perturbed compared to non-infected control subjects' plasma samples were identified. Among these 12 lipid classes, ether-linked phosphatidylcholines, ether-linked phosphatidylethanolamines, phosphatidylcholines, and ceramides were the four most perturbed. Pathway analysis revealed that the glycerophospholipid, sphingolipid, and ether lipid metabolisms pathway were the most significantly perturbed host pathways. Phosphatidic acid phosphatases (PAP) were involved in all three pathways and PAP-1 deficiency significantly suppressed SARS-CoV-2 replication. siRNA knockdown of LPIN2 and LPIN3 resulted in significant reduction of SARS-CoV-2 load. In summary, these findings characterized the host lipidomic changes upon SARS-CoV-2 infection and identified PAP-1 as a potential target for intervention for COVID-19.</abstract><cop>Sydney</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>35874954</pmid><doi>10.7150/ijbs.73057</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acid phosphatase Coronaviruses COVID-19 Lipid metabolism Lipids Liquid chromatography Mass spectrometry Mass spectroscopy Phosphatidic acid Phosphatidylethanolamine Replication Research Paper Severe acute respiratory syndrome coronavirus 2 siRNA Viral diseases Viruses |
| title | Phosphatidic acid phosphatase 1 impairs SARS-CoV-2 replication by affecting the glycerophospholipid metabolism pathway |
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