SARS‐CoV‐2‐encoded inhibitors of human LINE‐1 retrotransposition
The ongoing pandemic of severe acute respiratory coronavirus 2 (SARS‐CoV‐2) is causing a devastating impact on public health worldwide. However, details concerning the profound impact of SARS‐CoV‐2 on host cells remain elusive. Here, we investigated the effects of SARS‐CoV‐2‐encoded viral proteins o...
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| Veröffentlicht in: | Journal of medical virology 2023-01, Vol.95 (1), p.e28135-n/a |
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| creator | Li, Yan Yang, Jiaxin Shen, Siyu Wang, Wei Liu, Nian Guo, Haoran Wei, Wei |
| description | The ongoing pandemic of severe acute respiratory coronavirus 2 (SARS‐CoV‐2) is causing a devastating impact on public health worldwide. However, details concerning the profound impact of SARS‐CoV‐2 on host cells remain elusive. Here, we investigated the effects of SARS‐CoV‐2‐encoded viral proteins on the intracellular activity of long interspersed element 1 (L1) retrotransposons using well‐established reporter systems. Several nonstructural or accessory proteins (Nsps) of SARS‐CoV‐2 (i.e., Nsp1, Nsp3, Nsp5, and Nsp14) significantly suppress human L1 mobility, and these viral L1 inhibitors generate a complex network that modulates L1 transposition. Specifically, Nsp1 and Nsp14 inhibit the intracellular accumulation of L1 open reading frame proteins (ORF1p), whereas Nsp3, Nsp5, and Nsp14 repress the reverse transcriptase activity of L1 ORF2p. Given recent findings concerning the roles of L1 in antiviral immune activation and host genome instability, the anti‐L1 activities mediated by SARS‐CoV‐2‐encoded inhibitors suggest that SARS‐CoV‐2 employs different strategies to optimize the host genetic environment. |
| doi_str_mv | 10.1002/jmv.28135 |
| format | Article |
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However, details concerning the profound impact of SARS‐CoV‐2 on host cells remain elusive. Here, we investigated the effects of SARS‐CoV‐2‐encoded viral proteins on the intracellular activity of long interspersed element 1 (L1) retrotransposons using well‐established reporter systems. Several nonstructural or accessory proteins (Nsps) of SARS‐CoV‐2 (i.e., Nsp1, Nsp3, Nsp5, and Nsp14) significantly suppress human L1 mobility, and these viral L1 inhibitors generate a complex network that modulates L1 transposition. Specifically, Nsp1 and Nsp14 inhibit the intracellular accumulation of L1 open reading frame proteins (ORF1p), whereas Nsp3, Nsp5, and Nsp14 repress the reverse transcriptase activity of L1 ORF2p. Given recent findings concerning the roles of L1 in antiviral immune activation and host genome instability, the anti‐L1 activities mediated by SARS‐CoV‐2‐encoded inhibitors suggest that SARS‐CoV‐2 employs different strategies to optimize the host genetic environment.</description><identifier>ISSN: 0146-6615</identifier><identifier>EISSN: 1096-9071</identifier><identifier>DOI: 10.1002/jmv.28135</identifier><identifier>PMID: 36085352</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>coronavirus ; Coronaviruses ; COVID-19 - genetics ; Genomes ; Genomic instability ; Humans ; Immune response ; Inhibitors ; Intracellular ; LINE‐1 ; Long Interspersed Nucleotide Elements ; Pandemics ; Proteins ; Public health ; Retrotransposition ; retrotransposon ; RNA-directed DNA polymerase ; SARS-CoV-2 - genetics ; SARS-CoV-2 - metabolism ; SARS‐CoV‐2 ; Severe acute respiratory syndrome ; Severe acute respiratory syndrome coronavirus 2 ; Transposition ; Viral diseases ; Viral Nonstructural Proteins - genetics ; Viral Nonstructural Proteins - metabolism ; Viral Proteins - genetics ; Virology</subject><ispartof>Journal of medical virology, 2023-01, Vol.95 (1), p.e28135-n/a</ispartof><rights>2022 Wiley Periodicals LLC.</rights><rights>2023 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4435-c24d0283ab8b7db5fc790123ed555e995342107cbe6dd6f14ddce94854d27ade3</citedby><cites>FETCH-LOGICAL-c4435-c24d0283ab8b7db5fc790123ed555e995342107cbe6dd6f14ddce94854d27ade3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjmv.28135$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjmv.28135$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36085352$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yan</creatorcontrib><creatorcontrib>Yang, Jiaxin</creatorcontrib><creatorcontrib>Shen, Siyu</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Liu, Nian</creatorcontrib><creatorcontrib>Guo, Haoran</creatorcontrib><creatorcontrib>Wei, Wei</creatorcontrib><title>SARS‐CoV‐2‐encoded inhibitors of human LINE‐1 retrotransposition</title><title>Journal of medical virology</title><addtitle>J Med Virol</addtitle><description>The ongoing pandemic of severe acute respiratory coronavirus 2 (SARS‐CoV‐2) is causing a devastating impact on public health worldwide. However, details concerning the profound impact of SARS‐CoV‐2 on host cells remain elusive. Here, we investigated the effects of SARS‐CoV‐2‐encoded viral proteins on the intracellular activity of long interspersed element 1 (L1) retrotransposons using well‐established reporter systems. Several nonstructural or accessory proteins (Nsps) of SARS‐CoV‐2 (i.e., Nsp1, Nsp3, Nsp5, and Nsp14) significantly suppress human L1 mobility, and these viral L1 inhibitors generate a complex network that modulates L1 transposition. Specifically, Nsp1 and Nsp14 inhibit the intracellular accumulation of L1 open reading frame proteins (ORF1p), whereas Nsp3, Nsp5, and Nsp14 repress the reverse transcriptase activity of L1 ORF2p. Given recent findings concerning the roles of L1 in antiviral immune activation and host genome instability, the anti‐L1 activities mediated by SARS‐CoV‐2‐encoded inhibitors suggest that SARS‐CoV‐2 employs different strategies to optimize the host genetic environment.</description><subject>coronavirus</subject><subject>Coronaviruses</subject><subject>COVID-19 - genetics</subject><subject>Genomes</subject><subject>Genomic instability</subject><subject>Humans</subject><subject>Immune response</subject><subject>Inhibitors</subject><subject>Intracellular</subject><subject>LINE‐1</subject><subject>Long Interspersed Nucleotide Elements</subject><subject>Pandemics</subject><subject>Proteins</subject><subject>Public health</subject><subject>Retrotransposition</subject><subject>retrotransposon</subject><subject>RNA-directed DNA polymerase</subject><subject>SARS-CoV-2 - genetics</subject><subject>SARS-CoV-2 - metabolism</subject><subject>SARS‐CoV‐2</subject><subject>Severe acute respiratory syndrome</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Transposition</subject><subject>Viral diseases</subject><subject>Viral Nonstructural Proteins - genetics</subject><subject>Viral Nonstructural Proteins - metabolism</subject><subject>Viral Proteins - genetics</subject><subject>Virology</subject><issn>0146-6615</issn><issn>1096-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctO3DAUhq0KVAbaRV8ARWLTLgI-viXeVEIjykXTIpWWrZXEDuNRYg92QsWOR-AZeRIMAwgqsTg-i_Pp02_9CH0BvAsYk71Ff7VLSqD8A5oAliKXuIA1NMHARC4E8A20GeMCY1xKQj6iDSpwySknE3R0tv_77O7mdurP00vSGNd4bXRm3dzWdvAhZr7N5mNfuWx2_OsgIZAFMwQ_hMrFpY92sN59Qutt1UXz-Wlvob8_Dv5Mj_LZ6eHxdH-WN4xRnjeEaUxKWtVlXeiat00hMRBqNOfcSMkpI4CLpjZCa9EC07oxkpWcaVJU2tAt9H3lXY51b9LRpRidWgbbV-Fa-cqqtxdn5-rCX6mkLgtGk-DrkyD4y9HEQfU2NqbrKmf8GBUpgJRMikd05z904cfg0vcSJQAkAJOJ-raimuBjDKZ9CQNYPfSjUj_qsZ_Ebr9O_0I-F5KAvRXwz3bm-n2TOvl5vlLeA-9mnXg</recordid><startdate>202301</startdate><enddate>202301</enddate><creator>Li, Yan</creator><creator>Yang, Jiaxin</creator><creator>Shen, Siyu</creator><creator>Wang, Wei</creator><creator>Liu, Nian</creator><creator>Guo, Haoran</creator><creator>Wei, Wei</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>202301</creationdate><title>SARS‐CoV‐2‐encoded inhibitors of human LINE‐1 retrotransposition</title><author>Li, Yan ; Yang, Jiaxin ; Shen, Siyu ; Wang, Wei ; Liu, Nian ; Guo, Haoran ; Wei, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4435-c24d0283ab8b7db5fc790123ed555e995342107cbe6dd6f14ddce94854d27ade3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>coronavirus</topic><topic>Coronaviruses</topic><topic>COVID-19 - genetics</topic><topic>Genomes</topic><topic>Genomic instability</topic><topic>Humans</topic><topic>Immune response</topic><topic>Inhibitors</topic><topic>Intracellular</topic><topic>LINE‐1</topic><topic>Long Interspersed Nucleotide Elements</topic><topic>Pandemics</topic><topic>Proteins</topic><topic>Public health</topic><topic>Retrotransposition</topic><topic>retrotransposon</topic><topic>RNA-directed DNA polymerase</topic><topic>SARS-CoV-2 - genetics</topic><topic>SARS-CoV-2 - metabolism</topic><topic>SARS‐CoV‐2</topic><topic>Severe acute respiratory syndrome</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Transposition</topic><topic>Viral diseases</topic><topic>Viral Nonstructural Proteins - genetics</topic><topic>Viral Nonstructural Proteins - metabolism</topic><topic>Viral Proteins - genetics</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yan</creatorcontrib><creatorcontrib>Yang, Jiaxin</creatorcontrib><creatorcontrib>Shen, Siyu</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Liu, Nian</creatorcontrib><creatorcontrib>Guo, Haoran</creatorcontrib><creatorcontrib>Wei, Wei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of medical virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yan</au><au>Yang, Jiaxin</au><au>Shen, Siyu</au><au>Wang, Wei</au><au>Liu, Nian</au><au>Guo, Haoran</au><au>Wei, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SARS‐CoV‐2‐encoded inhibitors of human LINE‐1 retrotransposition</atitle><jtitle>Journal of medical virology</jtitle><addtitle>J Med Virol</addtitle><date>2023-01</date><risdate>2023</risdate><volume>95</volume><issue>1</issue><spage>e28135</spage><epage>n/a</epage><pages>e28135-n/a</pages><issn>0146-6615</issn><eissn>1096-9071</eissn><abstract>The ongoing pandemic of severe acute respiratory coronavirus 2 (SARS‐CoV‐2) is causing a devastating impact on public health worldwide. However, details concerning the profound impact of SARS‐CoV‐2 on host cells remain elusive. Here, we investigated the effects of SARS‐CoV‐2‐encoded viral proteins on the intracellular activity of long interspersed element 1 (L1) retrotransposons using well‐established reporter systems. Several nonstructural or accessory proteins (Nsps) of SARS‐CoV‐2 (i.e., Nsp1, Nsp3, Nsp5, and Nsp14) significantly suppress human L1 mobility, and these viral L1 inhibitors generate a complex network that modulates L1 transposition. Specifically, Nsp1 and Nsp14 inhibit the intracellular accumulation of L1 open reading frame proteins (ORF1p), whereas Nsp3, Nsp5, and Nsp14 repress the reverse transcriptase activity of L1 ORF2p. 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| subjects | coronavirus Coronaviruses COVID-19 - genetics Genomes Genomic instability Humans Immune response Inhibitors Intracellular LINE‐1 Long Interspersed Nucleotide Elements Pandemics Proteins Public health Retrotransposition retrotransposon RNA-directed DNA polymerase SARS-CoV-2 - genetics SARS-CoV-2 - metabolism SARS‐CoV‐2 Severe acute respiratory syndrome Severe acute respiratory syndrome coronavirus 2 Transposition Viral diseases Viral Nonstructural Proteins - genetics Viral Nonstructural Proteins - metabolism Viral Proteins - genetics Virology |
| title | SARS‐CoV‐2‐encoded inhibitors of human LINE‐1 retrotransposition |
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