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SFTS phlebovirus promotes LC3-II accumulation and nonstructural protein of SFTS phlebovirus co-localizes with autophagy proteins
Autophagy is essential for eukaryotic cell homeostasis and can perform both anti-viral and pro-viral roles depending on the kinds of viruses, cell types and cell environment. Severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) is a newly discovered tick-borne virus in the Phenuiviridae f...
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Published in: | Scientific reports 2018-03, Vol.8 (1), p.5287-11, Article 5287 |
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description | Autophagy is essential for eukaryotic cell homeostasis and can perform both anti-viral and pro-viral roles depending on the kinds of viruses, cell types and cell environment. Severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) is a newly discovered tick-borne virus in the
Phenuiviridae
family that causes a severe hemorrhagic fever disease in East Asia. In this study we determined interactions between SFTSV and autophagy. Our results showed that LC3-II (microtubule associated protein 1 light chain 3-II) protein accumulated from 4 h to 24 h after SFTSV infection compared to mock-infected Vero cells, and the use of E64d and pepstatin A did not affect the expression of LC3-II protein, which indicated that the increased LC3-II may be the result of inhibition of autophagic degradation caused by SFTSV infection. However, knockdown of
LC3B
promotes SFTSV replication, which indicated a negative role of LC3B protein in SFTSV replication. We also detected co-localization of SFTSV non-structure (NSs) protein with LC3B, p62 and Lamp2b respectively in SFTSV infected Vero cells, which indicated the possibility of selective autophagy or chaperone-mediated autophagy involving in SFTSV infection. Our results indicated that SFTSV infection promotes LC3 accumulation and several proteins of the autophagy pathway co-localize with NSs protein during SFTSV infection. |
doi_str_mv | 10.1038/s41598-018-23610-0 |
format | article |
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Phenuiviridae
family that causes a severe hemorrhagic fever disease in East Asia. In this study we determined interactions between SFTSV and autophagy. Our results showed that LC3-II (microtubule associated protein 1 light chain 3-II) protein accumulated from 4 h to 24 h after SFTSV infection compared to mock-infected Vero cells, and the use of E64d and pepstatin A did not affect the expression of LC3-II protein, which indicated that the increased LC3-II may be the result of inhibition of autophagic degradation caused by SFTSV infection. However, knockdown of
LC3B
promotes SFTSV replication, which indicated a negative role of LC3B protein in SFTSV replication. We also detected co-localization of SFTSV non-structure (NSs) protein with LC3B, p62 and Lamp2b respectively in SFTSV infected Vero cells, which indicated the possibility of selective autophagy or chaperone-mediated autophagy involving in SFTSV infection. Our results indicated that SFTSV infection promotes LC3 accumulation and several proteins of the autophagy pathway co-localize with NSs protein during SFTSV infection.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-23610-0</identifier><identifier>PMID: 29588492</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/89 ; 14 ; 14/19 ; 14/32 ; 59 ; 631/326 ; 631/326/596 ; 631/326/596/2553 ; 64 ; 82/1 ; Antiviral agents ; Autophagy ; Biodegradation ; Hemorrhage ; Hemorrhagic fever ; Homeostasis ; Humanities and Social Sciences ; Infections ; Localization ; multidisciplinary ; Phagocytosis ; Protein structure ; Proteins ; Replication ; Science ; Science (multidisciplinary) ; Thrombocytopenia ; Vero cells</subject><ispartof>Scientific reports, 2018-03, Vol.8 (1), p.5287-11, Article 5287</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-333238f7be23510912880eb05c1f7b902ead62e813f3c615f1c801cbf6e796593</citedby><cites>FETCH-LOGICAL-c511t-333238f7be23510912880eb05c1f7b902ead62e813f3c615f1c801cbf6e796593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2019027887/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2019027887?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29588492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Yue</creatorcontrib><creatorcontrib>Liu, Miao-miao</creatorcontrib><creatorcontrib>Lei, Xiao-ying</creatorcontrib><creatorcontrib>Yu, Xue-jie</creatorcontrib><title>SFTS phlebovirus promotes LC3-II accumulation and nonstructural protein of SFTS phlebovirus co-localizes with autophagy proteins</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Autophagy is essential for eukaryotic cell homeostasis and can perform both anti-viral and pro-viral roles depending on the kinds of viruses, cell types and cell environment. Severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) is a newly discovered tick-borne virus in the
Phenuiviridae
family that causes a severe hemorrhagic fever disease in East Asia. In this study we determined interactions between SFTSV and autophagy. Our results showed that LC3-II (microtubule associated protein 1 light chain 3-II) protein accumulated from 4 h to 24 h after SFTSV infection compared to mock-infected Vero cells, and the use of E64d and pepstatin A did not affect the expression of LC3-II protein, which indicated that the increased LC3-II may be the result of inhibition of autophagic degradation caused by SFTSV infection. However, knockdown of
LC3B
promotes SFTSV replication, which indicated a negative role of LC3B protein in SFTSV replication. We also detected co-localization of SFTSV non-structure (NSs) protein with LC3B, p62 and Lamp2b respectively in SFTSV infected Vero cells, which indicated the possibility of selective autophagy or chaperone-mediated autophagy involving in SFTSV infection. Our results indicated that SFTSV infection promotes LC3 accumulation and several proteins of the autophagy pathway co-localize with NSs protein during SFTSV infection.</description><subject>13/109</subject><subject>13/89</subject><subject>14</subject><subject>14/19</subject><subject>14/32</subject><subject>59</subject><subject>631/326</subject><subject>631/326/596</subject><subject>631/326/596/2553</subject><subject>64</subject><subject>82/1</subject><subject>Antiviral agents</subject><subject>Autophagy</subject><subject>Biodegradation</subject><subject>Hemorrhage</subject><subject>Hemorrhagic fever</subject><subject>Homeostasis</subject><subject>Humanities and Social Sciences</subject><subject>Infections</subject><subject>Localization</subject><subject>multidisciplinary</subject><subject>Phagocytosis</subject><subject>Protein structure</subject><subject>Proteins</subject><subject>Replication</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Thrombocytopenia</subject><subject>Vero cells</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNp9kc9rFDEUx0NRbKn9BzyUgBcvo3nJZDa5CLJYXVjw0HoOmWxmN2UmGfOjUk_-6abdtlYLDYS85H3eN-_xRegNkPdAmPiQWuBSNAREQ1kHpCEH6IiSltcrpS8exYfoJKVLUhensgX5Ch1SyYVoJT1Cv8_PLs7xvBttH65cLAnPMUwh24TXS9asVlgbU6Yy6uyCx9pvsA8-5VhMLlGPN3i2zuMw4CdSJjRjMHp0v6rcT5d3WJcc5p3eXt_Xpdfo5aDHZE_uzmP0_ezzxfJrs_72ZbX8tG4MB8gNY4wyMSx6SxkHIoEKQWxPuIH6KAm1etNRK4ANzHTABzCCgOmHzi5kxyU7Rh_3unPpJ7sx1ufavpqjm3S8VkE79W_Gu53ahivFRSe5hCrw7k4ghh_Fpqwml4wdR-1tKElRArLtZN0VffsfehlK9HW8W4rQhRCLStE9ZWJIKdrhoRkg6sZjtfdYVY_VrceK1KLTx2M8lNw7WgG2B1JN-a2Nf_9-RvYPiNGzzQ</recordid><startdate>20180327</startdate><enddate>20180327</enddate><creator>Sun, Yue</creator><creator>Liu, Miao-miao</creator><creator>Lei, Xiao-ying</creator><creator>Yu, Xue-jie</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180327</creationdate><title>SFTS phlebovirus promotes LC3-II accumulation and nonstructural protein of SFTS phlebovirus co-localizes with autophagy proteins</title><author>Sun, Yue ; Liu, Miao-miao ; Lei, Xiao-ying ; Yu, Xue-jie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-333238f7be23510912880eb05c1f7b902ead62e813f3c615f1c801cbf6e796593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>13/109</topic><topic>13/89</topic><topic>14</topic><topic>14/19</topic><topic>14/32</topic><topic>59</topic><topic>631/326</topic><topic>631/326/596</topic><topic>631/326/596/2553</topic><topic>64</topic><topic>82/1</topic><topic>Antiviral agents</topic><topic>Autophagy</topic><topic>Biodegradation</topic><topic>Hemorrhage</topic><topic>Hemorrhagic fever</topic><topic>Homeostasis</topic><topic>Humanities and Social Sciences</topic><topic>Infections</topic><topic>Localization</topic><topic>multidisciplinary</topic><topic>Phagocytosis</topic><topic>Protein structure</topic><topic>Proteins</topic><topic>Replication</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Thrombocytopenia</topic><topic>Vero cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Yue</creatorcontrib><creatorcontrib>Liu, Miao-miao</creatorcontrib><creatorcontrib>Lei, Xiao-ying</creatorcontrib><creatorcontrib>Yu, Xue-jie</creatorcontrib><collection>SpringerOpen</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Yue</au><au>Liu, Miao-miao</au><au>Lei, Xiao-ying</au><au>Yu, Xue-jie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SFTS phlebovirus promotes LC3-II accumulation and nonstructural protein of SFTS phlebovirus co-localizes with autophagy proteins</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-03-27</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>5287</spage><epage>11</epage><pages>5287-11</pages><artnum>5287</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Autophagy is essential for eukaryotic cell homeostasis and can perform both anti-viral and pro-viral roles depending on the kinds of viruses, cell types and cell environment. Severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) is a newly discovered tick-borne virus in the
Phenuiviridae
family that causes a severe hemorrhagic fever disease in East Asia. In this study we determined interactions between SFTSV and autophagy. Our results showed that LC3-II (microtubule associated protein 1 light chain 3-II) protein accumulated from 4 h to 24 h after SFTSV infection compared to mock-infected Vero cells, and the use of E64d and pepstatin A did not affect the expression of LC3-II protein, which indicated that the increased LC3-II may be the result of inhibition of autophagic degradation caused by SFTSV infection. However, knockdown of
LC3B
promotes SFTSV replication, which indicated a negative role of LC3B protein in SFTSV replication. We also detected co-localization of SFTSV non-structure (NSs) protein with LC3B, p62 and Lamp2b respectively in SFTSV infected Vero cells, which indicated the possibility of selective autophagy or chaperone-mediated autophagy involving in SFTSV infection. Our results indicated that SFTSV infection promotes LC3 accumulation and several proteins of the autophagy pathway co-localize with NSs protein during SFTSV infection.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29588492</pmid><doi>10.1038/s41598-018-23610-0</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13/109 13/89 14 14/19 14/32 59 631/326 631/326/596 631/326/596/2553 64 82/1 Antiviral agents Autophagy Biodegradation Hemorrhage Hemorrhagic fever Homeostasis Humanities and Social Sciences Infections Localization multidisciplinary Phagocytosis Protein structure Proteins Replication Science Science (multidisciplinary) Thrombocytopenia Vero cells |
title | SFTS phlebovirus promotes LC3-II accumulation and nonstructural protein of SFTS phlebovirus co-localizes with autophagy proteins |
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