Alteration of Antiviral Signalling by Single Nucleotide Polymorphisms (SNPs) of Mitochondrial Antiviral Signalling Protein (MAVS)
Genetic variation is associated with diseases. As a type of genetic variation occurring with certain regularity and frequency, the single nucleotide polymorphism (SNP) is attracting more and more attention because of its great value for research and real-life application. Mitochondrial antiviral sig...
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| creator | Xing, Fei Matsumiya, Tomoh Hayakari, Ryo Yoshida, Hidemi Kawaguchi, Shogo Takahashi, Ippei Nakaji, Shigeyuki Imaizumi, Tadaatsu |
| description | Genetic variation is associated with diseases. As a type of genetic variation occurring with certain regularity and frequency, the single nucleotide polymorphism (SNP) is attracting more and more attention because of its great value for research and real-life application. Mitochondrial antiviral signalling protein (MAVS) acts as a common adaptor molecule for retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), which can recognize foreign RNA, including viral RNA, leading to the induction of type I interferons (IFNs). Therefore, MAVS is thought to be a crucial molecule in antiviral innate immunity. We speculated that genetic variation of MAVS may result in susceptibility to infectious diseases. To assess the risk of viral infection based on MAVS variation, we tested the effects of twelve non-synonymous MAVS coding-region SNPs from the National Center for Biotechnology Information (NCBI) database that result in amino acid substitutions. We found that five of these SNPs exhibited functional alterations. Additionally, four resulted in an inhibitory immune response, and one had the opposite effect. In total, 1,032 human genomic samples obtained from a mass examination were genotyped at these five SNPs. However, no homozygous or heterozygous variation was detected. We hypothesized that these five SNPs are not present in the Japanese population and that such MAVS variations may result in serious immune diseases. |
| doi_str_mv | 10.1371/journal.pone.0151173 |
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As a type of genetic variation occurring with certain regularity and frequency, the single nucleotide polymorphism (SNP) is attracting more and more attention because of its great value for research and real-life application. Mitochondrial antiviral signalling protein (MAVS) acts as a common adaptor molecule for retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), which can recognize foreign RNA, including viral RNA, leading to the induction of type I interferons (IFNs). Therefore, MAVS is thought to be a crucial molecule in antiviral innate immunity. We speculated that genetic variation of MAVS may result in susceptibility to infectious diseases. To assess the risk of viral infection based on MAVS variation, we tested the effects of twelve non-synonymous MAVS coding-region SNPs from the National Center for Biotechnology Information (NCBI) database that result in amino acid substitutions. We found that five of these SNPs exhibited functional alterations. Additionally, four resulted in an inhibitory immune response, and one had the opposite effect. In total, 1,032 human genomic samples obtained from a mass examination were genotyped at these five SNPs. However, no homozygous or heterozygous variation was detected. We hypothesized that these five SNPs are not present in the Japanese population and that such MAVS variations may result in serious immune diseases.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0151173</identifier><identifier>PMID: 26954674</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acids ; Adaptor Proteins, Signal Transducing - genetics ; Alleles ; Amino Acid Substitution ; Amino acids ; Antiviral drugs ; Biology ; Biology and Life Sciences ; Biotechnology ; Cellular signal transduction ; Cloning ; Databases, Genetic ; Gene Frequency ; Genes ; Genetic aspects ; Genetic diversity ; Genetic Variation ; Genotype ; Health aspects ; Health risks ; HeLa Cells ; Hepatitis ; Humans ; Immune response ; Immune system ; Immunity ; Immunological diseases ; Infectious diseases ; Innate immunity ; Interferon ; Intracellular Space ; Kinases ; Laboratories ; Medicine ; Medicine and Health Sciences ; Mitochondria ; Mitochondrial Proteins - genetics ; Mutagenesis ; Phosphorylation ; Poly I-C - pharmacology ; Polymorphism ; Polymorphism, Single Nucleotide ; Properties ; Protein Transport ; Proteins ; Receptors ; Research and Analysis Methods ; Retinoic acid ; Ribonucleic acid ; Risk assessment ; Risk factors ; RNA ; Science ; Signal Transduction - drug effects ; Signaling ; Signaling peptides and proteins ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Staphylococcus infections ; University graduates ; Vectors (Biology) ; Viral infections ; Virus diseases ; Viruses</subject><ispartof>PloS one, 2016-03, Vol.11 (3), p.e0151173-e0151173</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Xing et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Xing et al 2016 Xing et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-e9aa353bb4621f56ea34de39e77cba44b693bc3ef65ff4ccaac7b6cdb47a48e33</citedby><cites>FETCH-LOGICAL-c557t-e9aa353bb4621f56ea34de39e77cba44b693bc3ef65ff4ccaac7b6cdb47a48e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783065/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783065/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26954674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Horner, Stacy M</contributor><creatorcontrib>Xing, Fei</creatorcontrib><creatorcontrib>Matsumiya, Tomoh</creatorcontrib><creatorcontrib>Hayakari, Ryo</creatorcontrib><creatorcontrib>Yoshida, Hidemi</creatorcontrib><creatorcontrib>Kawaguchi, Shogo</creatorcontrib><creatorcontrib>Takahashi, Ippei</creatorcontrib><creatorcontrib>Nakaji, Shigeyuki</creatorcontrib><creatorcontrib>Imaizumi, Tadaatsu</creatorcontrib><title>Alteration of Antiviral Signalling by Single Nucleotide Polymorphisms (SNPs) of Mitochondrial Antiviral Signalling Protein (MAVS)</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Genetic variation is associated with diseases. As a type of genetic variation occurring with certain regularity and frequency, the single nucleotide polymorphism (SNP) is attracting more and more attention because of its great value for research and real-life application. Mitochondrial antiviral signalling protein (MAVS) acts as a common adaptor molecule for retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), which can recognize foreign RNA, including viral RNA, leading to the induction of type I interferons (IFNs). Therefore, MAVS is thought to be a crucial molecule in antiviral innate immunity. We speculated that genetic variation of MAVS may result in susceptibility to infectious diseases. To assess the risk of viral infection based on MAVS variation, we tested the effects of twelve non-synonymous MAVS coding-region SNPs from the National Center for Biotechnology Information (NCBI) database that result in amino acid substitutions. We found that five of these SNPs exhibited functional alterations. Additionally, four resulted in an inhibitory immune response, and one had the opposite effect. In total, 1,032 human genomic samples obtained from a mass examination were genotyped at these five SNPs. However, no homozygous or heterozygous variation was detected. We hypothesized that these five SNPs are not present in the Japanese population and that such MAVS variations may result in serious immune diseases.</description><subject>Acids</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Alleles</subject><subject>Amino Acid Substitution</subject><subject>Amino acids</subject><subject>Antiviral drugs</subject><subject>Biology</subject><subject>Biology and Life Sciences</subject><subject>Biotechnology</subject><subject>Cellular signal transduction</subject><subject>Cloning</subject><subject>Databases, Genetic</subject><subject>Gene Frequency</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic diversity</subject><subject>Genetic Variation</subject><subject>Genotype</subject><subject>Health aspects</subject><subject>Health risks</subject><subject>HeLa Cells</subject><subject>Hepatitis</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunological diseases</subject><subject>Infectious diseases</subject><subject>Innate immunity</subject><subject>Interferon</subject><subject>Intracellular Space</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mitochondria</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mutagenesis</subject><subject>Phosphorylation</subject><subject>Poly I-C - pharmacology</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Properties</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Research and Analysis Methods</subject><subject>Retinoic acid</subject><subject>Ribonucleic acid</subject><subject>Risk assessment</subject><subject>Risk factors</subject><subject>RNA</subject><subject>Science</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Signaling peptides and proteins</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Staphylococcus infections</subject><subject>University graduates</subject><subject>Vectors (Biology)</subject><subject>Viral infections</subject><subject>Virus diseases</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkl9v0zAUxSMEYmPwDRBEQkLdQ0scO3byghRNAyZto1KBV8t2blJXrl1sZ1If-eZz127a0J787_jne49Plr1HxQxhhr6s3OitMLONszArUIUQwy-yY9TgckrLAr98ND_K3oSwKooK15S-zo5K2lSEMnKc_WtNBC-idjZ3fd7aqG-0FyZf6CHRjbZDLrdpZQcD-fWoDLioO8jnzmzXzm-WOqxDPllcz8PpjnClo1NLZzuvE-VZ3ty7CNrmk6v2z-L0bfaqFybAu8N4kv3-dv7r7Mf08uf3i7P2cqqqisUpNELgCktJaIn6ioLApAPcAGNKCkIkbbBUGHpa9T1RSgjFJFWdJEyQGjA-yT7uuRvjAj-4FzhiDBFCCUZJcbFXdE6s-MbrtfBb7oTmdxvOD1z4qJMFXGHRsUJiIGVNSsIaWnZdXcsO-rIRSCTW18Nro1xDp8DG5MIT6NMTq5d8cDecsBoXtEqAyQHg3d8RQuRrHRQYIyy48a7uEhGKijpJP_0nfb67z3vVIFIDSxAmLoMz4-7rA29JldxFBDdJSPZC5V0IHvqHqlHBd9G7x_Nd9Pgheunah8cdP1y6zxq-BZk62Tk</recordid><startdate>20160308</startdate><enddate>20160308</enddate><creator>Xing, Fei</creator><creator>Matsumiya, Tomoh</creator><creator>Hayakari, Ryo</creator><creator>Yoshida, Hidemi</creator><creator>Kawaguchi, Shogo</creator><creator>Takahashi, Ippei</creator><creator>Nakaji, Shigeyuki</creator><creator>Imaizumi, Tadaatsu</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160308</creationdate><title>Alteration of Antiviral Signalling by Single Nucleotide Polymorphisms (SNPs) of Mitochondrial Antiviral Signalling Protein (MAVS)</title><author>Xing, Fei ; Matsumiya, Tomoh ; Hayakari, Ryo ; Yoshida, Hidemi ; Kawaguchi, Shogo ; Takahashi, Ippei ; Nakaji, Shigeyuki ; Imaizumi, Tadaatsu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c557t-e9aa353bb4621f56ea34de39e77cba44b693bc3ef65ff4ccaac7b6cdb47a48e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acids</topic><topic>Adaptor Proteins, Signal Transducing - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xing, Fei</au><au>Matsumiya, Tomoh</au><au>Hayakari, Ryo</au><au>Yoshida, Hidemi</au><au>Kawaguchi, Shogo</au><au>Takahashi, Ippei</au><au>Nakaji, Shigeyuki</au><au>Imaizumi, Tadaatsu</au><au>Horner, Stacy M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alteration of Antiviral Signalling by Single Nucleotide Polymorphisms (SNPs) of Mitochondrial Antiviral Signalling Protein (MAVS)</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-03-08</date><risdate>2016</risdate><volume>11</volume><issue>3</issue><spage>e0151173</spage><epage>e0151173</epage><pages>e0151173-e0151173</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Genetic variation is associated with diseases. As a type of genetic variation occurring with certain regularity and frequency, the single nucleotide polymorphism (SNP) is attracting more and more attention because of its great value for research and real-life application. Mitochondrial antiviral signalling protein (MAVS) acts as a common adaptor molecule for retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), which can recognize foreign RNA, including viral RNA, leading to the induction of type I interferons (IFNs). Therefore, MAVS is thought to be a crucial molecule in antiviral innate immunity. We speculated that genetic variation of MAVS may result in susceptibility to infectious diseases. To assess the risk of viral infection based on MAVS variation, we tested the effects of twelve non-synonymous MAVS coding-region SNPs from the National Center for Biotechnology Information (NCBI) database that result in amino acid substitutions. We found that five of these SNPs exhibited functional alterations. Additionally, four resulted in an inhibitory immune response, and one had the opposite effect. In total, 1,032 human genomic samples obtained from a mass examination were genotyped at these five SNPs. However, no homozygous or heterozygous variation was detected. We hypothesized that these five SNPs are not present in the Japanese population and that such MAVS variations may result in serious immune diseases.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26954674</pmid><doi>10.1371/journal.pone.0151173</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Acids Adaptor Proteins, Signal Transducing - genetics Alleles Amino Acid Substitution Amino acids Antiviral drugs Biology Biology and Life Sciences Biotechnology Cellular signal transduction Cloning Databases, Genetic Gene Frequency Genes Genetic aspects Genetic diversity Genetic Variation Genotype Health aspects Health risks HeLa Cells Hepatitis Humans Immune response Immune system Immunity Immunological diseases Infectious diseases Innate immunity Interferon Intracellular Space Kinases Laboratories Medicine Medicine and Health Sciences Mitochondria Mitochondrial Proteins - genetics Mutagenesis Phosphorylation Poly I-C - pharmacology Polymorphism Polymorphism, Single Nucleotide Properties Protein Transport Proteins Receptors Research and Analysis Methods Retinoic acid Ribonucleic acid Risk assessment Risk factors RNA Science Signal Transduction - drug effects Signaling Signaling peptides and proteins Single nucleotide polymorphisms Single-nucleotide polymorphism Staphylococcus infections University graduates Vectors (Biology) Viral infections Virus diseases Viruses |
| title | Alteration of Antiviral Signalling by Single Nucleotide Polymorphisms (SNPs) of Mitochondrial Antiviral Signalling Protein (MAVS) |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T19%3A20%3A55IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Alteration%20of%20Antiviral%20Signalling%20by%20Single%20Nucleotide%20Polymorphisms%20(SNPs)%20of%20Mitochondrial%20Antiviral%20Signalling%20Protein%20(MAVS)&rft.jtitle=PloS%20one&rft.au=Xing,%20Fei&rft.date=2016-03-08&rft.volume=11&rft.issue=3&rft.spage=e0151173&rft.epage=e0151173&rft.pages=e0151173-e0151173&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0151173&rft_dat=%3Cgale_plos_%3EA453531439%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1771446431&rft_id=info:pmid/26954674&rft_galeid=A453531439&rft_doaj_id=oai_doaj_org_article_c3ad70b3e4284247962dd88bdef29a1a&rfr_iscdi=true |