Polymorphisms of the prion gene promoter region that influence classical bovine spongiform encephalopathy susceptibility are not applicable to other transmissible spongiform encephalopathies in cattle
Two regulatory region polymorphisms in the prion gene of cattle have been reported to have an association with resistance to classical bovine spongiform encephalopathy (BSE). However, it is not known if this association also applies to other transmissible spongiform encephalopathies (TSE) in cattle....
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Veröffentlicht in: | Journal of animal science 2007-12, Vol.85 (12), p.3142-3147 |
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creator | Brunelle, B.W Hamir, A.N Baron, T Biacabe, A.G Richt, J.A Kunkle, R.A Cutlip, R.C Miller, J.M Nicholson, E.M |
description | Two regulatory region polymorphisms in the prion gene of cattle have been reported to have an association with resistance to classical bovine spongiform encephalopathy (BSE). However, it is not known if this association also applies to other transmissible spongiform encephalopathies (TSE) in cattle. In this report, we compare the relationship between these 2 polymorphisms and resistance in cattle affected with naturally occurring atypical BSE as well as in cattle experimentally inoculated with either scrapie, chronic wasting disease, or transmissible mink encephalopathy. Our analysis revealed no association between genotype and resistance to atypical BSE or experimentally inoculated TSE. This indicates the promoter polymorphism correlation is specific to classical BSE and that atypical BSE and experimentally inoculated TSE are bypassing the site of influence of the polymorphisms. This genetic discrepancy demonstrates that atypical BSE progresses differently in the host relative to classical BSE. These results are consistent with the notion that atypical BSE originates spontaneously in cattle. |
doi_str_mv | 10.2527/jas.2007-0208 |
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However, it is not known if this association also applies to other transmissible spongiform encephalopathies (TSE) in cattle. In this report, we compare the relationship between these 2 polymorphisms and resistance in cattle affected with naturally occurring atypical BSE as well as in cattle experimentally inoculated with either scrapie, chronic wasting disease, or transmissible mink encephalopathy. Our analysis revealed no association between genotype and resistance to atypical BSE or experimentally inoculated TSE. This indicates the promoter polymorphism correlation is specific to classical BSE and that atypical BSE and experimentally inoculated TSE are bypassing the site of influence of the polymorphisms. This genetic discrepancy demonstrates that atypical BSE progresses differently in the host relative to classical BSE. These results are consistent with the notion that atypical BSE originates spontaneously in cattle.</description><identifier>ISSN: 0021-8812</identifier><identifier>EISSN: 1525-3163</identifier><identifier>DOI: 10.2527/jas.2007-0208</identifier><identifier>PMID: 17709775</identifier><language>eng</language><publisher>Savoy, IL: American Society of Animal Science</publisher><subject>Animal productions ; Animals ; atypical bovine spongiform encephalopathy ; Biological and medical sciences ; Bovine spongiform encephalopathy ; Cattle ; Cattle Diseases - genetics ; chronic wasting disease ; disease resistance ; Disease Susceptibility - veterinary ; disease transmission ; Encephalopathy, Bovine Spongiform - genetics ; epidemiology ; Fundamental and applied biological sciences. Psychology ; genes ; genetic polymorphism ; Genetic Predisposition to Disease ; genetic resistance ; Genotype ; Genotype & phenotype ; molecular sequence data ; Polymorphism ; Polymorphism, Genetic ; prion diseases ; Prion Diseases - genetics ; Prions ; Prions - genetics ; promoter regions ; Promoter Regions, Genetic ; scrapie ; Species Specificity ; Spongiform encephalopathies ; Terrestrial animal productions ; transmissible mink encephalopathy ; Vertebrates</subject><ispartof>Journal of animal science, 2007-12, Vol.85 (12), p.3142-3147</ispartof><rights>2008 INIST-CNRS</rights><rights>Copyright American Society of Animal Science Dec 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19876322$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17709775$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brunelle, B.W</creatorcontrib><creatorcontrib>Hamir, A.N</creatorcontrib><creatorcontrib>Baron, T</creatorcontrib><creatorcontrib>Biacabe, A.G</creatorcontrib><creatorcontrib>Richt, J.A</creatorcontrib><creatorcontrib>Kunkle, R.A</creatorcontrib><creatorcontrib>Cutlip, R.C</creatorcontrib><creatorcontrib>Miller, J.M</creatorcontrib><creatorcontrib>Nicholson, E.M</creatorcontrib><title>Polymorphisms of the prion gene promoter region that influence classical bovine spongiform encephalopathy susceptibility are not applicable to other transmissible spongiform encephalopathies in cattle</title><title>Journal of animal science</title><addtitle>J Anim Sci</addtitle><description>Two regulatory region polymorphisms in the prion gene of cattle have been reported to have an association with resistance to classical bovine spongiform encephalopathy (BSE). However, it is not known if this association also applies to other transmissible spongiform encephalopathies (TSE) in cattle. In this report, we compare the relationship between these 2 polymorphisms and resistance in cattle affected with naturally occurring atypical BSE as well as in cattle experimentally inoculated with either scrapie, chronic wasting disease, or transmissible mink encephalopathy. Our analysis revealed no association between genotype and resistance to atypical BSE or experimentally inoculated TSE. This indicates the promoter polymorphism correlation is specific to classical BSE and that atypical BSE and experimentally inoculated TSE are bypassing the site of influence of the polymorphisms. This genetic discrepancy demonstrates that atypical BSE progresses differently in the host relative to classical BSE. These results are consistent with the notion that atypical BSE originates spontaneously in cattle.</description><subject>Animal productions</subject><subject>Animals</subject><subject>atypical bovine spongiform encephalopathy</subject><subject>Biological and medical sciences</subject><subject>Bovine spongiform encephalopathy</subject><subject>Cattle</subject><subject>Cattle Diseases - genetics</subject><subject>chronic wasting disease</subject><subject>disease resistance</subject><subject>Disease Susceptibility - veterinary</subject><subject>disease transmission</subject><subject>Encephalopathy, Bovine Spongiform - genetics</subject><subject>epidemiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>genes</subject><subject>genetic polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>genetic resistance</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>molecular sequence data</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>prion diseases</subject><subject>Prion Diseases - genetics</subject><subject>Prions</subject><subject>Prions - genetics</subject><subject>promoter regions</subject><subject>Promoter Regions, Genetic</subject><subject>scrapie</subject><subject>Species Specificity</subject><subject>Spongiform encephalopathies</subject><subject>Terrestrial animal productions</subject><subject>transmissible mink encephalopathy</subject><subject>Vertebrates</subject><issn>0021-8812</issn><issn>1525-3163</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkluL1DAUgIso7uzqo68aBPWpa66T9HFZXBUWFHSfy2k2nWZIm5qkyvxDf5anzIggiE9JDh_fuaWqnjF6yRXXb_eQLzmluqacmgfVhimuasG24mG1oZSz2hjGz6rznPeUMq4a9bg6Y1rTRmu1qX5-juEwxjQPPo-ZxJ6UwZE5-TiRnZvWaxxjcYkkt1uDZYBC_NSHxU3WERsgZ28hkC5-98jnOU4738c0khWYBwhxhjIcSF4yvovvfPDlQCA5MsVCYJ4DCrrgSIkkYvpESoIpjx7Na_hfSu8yVkIslBLck-pRDyG7p6fzorq7eff1-kN9--n9x-ur27oXSpSaaeid7XrZSKGMsEaZrukN185KznmHk6MShJQOHKitcfcdh05RIXUjqbXionp99OJgvi0ulxbrtC4EmFxccrs1SlCB9v-BnGqKeQWCL_8C93FJEzbRcmaYZI02CD0_QUs3uvsWNzRCOrS_N4nAqxMAGdfR4wStz3-4xuit4By5N0du8Lvhh0-uzSOEgFrW4l8yqmW8FUyu5Isj2UNsYZfQdveFUyboWveWS_ELedbJrw</recordid><startdate>20071201</startdate><enddate>20071201</enddate><creator>Brunelle, B.W</creator><creator>Hamir, A.N</creator><creator>Baron, T</creator><creator>Biacabe, A.G</creator><creator>Richt, J.A</creator><creator>Kunkle, R.A</creator><creator>Cutlip, R.C</creator><creator>Miller, J.M</creator><creator>Nicholson, E.M</creator><general>American Society of Animal Science</general><general>Am Soc Animal Sci</general><general>Oxford University Press</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7RQ</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>M7S</scope><scope>MBDVC</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>S0X</scope><scope>U9A</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20071201</creationdate><title>Polymorphisms of the prion gene promoter region that influence classical bovine spongiform encephalopathy susceptibility are not applicable to other transmissible spongiform encephalopathies in cattle</title><author>Brunelle, B.W ; Hamir, A.N ; Baron, T ; Biacabe, A.G ; Richt, J.A ; Kunkle, R.A ; Cutlip, R.C ; Miller, J.M ; Nicholson, E.M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-f353t-17afecbf4943583c858b9f827ec4222b31604a344eaea568edb2ab50347940cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animal productions</topic><topic>Animals</topic><topic>atypical bovine spongiform encephalopathy</topic><topic>Biological and medical sciences</topic><topic>Bovine spongiform encephalopathy</topic><topic>Cattle</topic><topic>Cattle Diseases - genetics</topic><topic>chronic wasting disease</topic><topic>disease resistance</topic><topic>Disease Susceptibility - veterinary</topic><topic>disease transmission</topic><topic>Encephalopathy, Bovine Spongiform - genetics</topic><topic>epidemiology</topic><topic>Fundamental and applied biological sciences. 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Academic</collection><jtitle>Journal of animal science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brunelle, B.W</au><au>Hamir, A.N</au><au>Baron, T</au><au>Biacabe, A.G</au><au>Richt, J.A</au><au>Kunkle, R.A</au><au>Cutlip, R.C</au><au>Miller, J.M</au><au>Nicholson, E.M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polymorphisms of the prion gene promoter region that influence classical bovine spongiform encephalopathy susceptibility are not applicable to other transmissible spongiform encephalopathies in cattle</atitle><jtitle>Journal of animal science</jtitle><addtitle>J Anim Sci</addtitle><date>2007-12-01</date><risdate>2007</risdate><volume>85</volume><issue>12</issue><spage>3142</spage><epage>3147</epage><pages>3142-3147</pages><issn>0021-8812</issn><eissn>1525-3163</eissn><abstract>Two regulatory region polymorphisms in the prion gene of cattle have been reported to have an association with resistance to classical bovine spongiform encephalopathy (BSE). However, it is not known if this association also applies to other transmissible spongiform encephalopathies (TSE) in cattle. In this report, we compare the relationship between these 2 polymorphisms and resistance in cattle affected with naturally occurring atypical BSE as well as in cattle experimentally inoculated with either scrapie, chronic wasting disease, or transmissible mink encephalopathy. Our analysis revealed no association between genotype and resistance to atypical BSE or experimentally inoculated TSE. This indicates the promoter polymorphism correlation is specific to classical BSE and that atypical BSE and experimentally inoculated TSE are bypassing the site of influence of the polymorphisms. This genetic discrepancy demonstrates that atypical BSE progresses differently in the host relative to classical BSE. These results are consistent with the notion that atypical BSE originates spontaneously in cattle.</abstract><cop>Savoy, IL</cop><pub>American Society of Animal Science</pub><pmid>17709775</pmid><doi>10.2527/jas.2007-0208</doi><tpages>6</tpages></addata></record> |
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subjects | Animal productions Animals atypical bovine spongiform encephalopathy Biological and medical sciences Bovine spongiform encephalopathy Cattle Cattle Diseases - genetics chronic wasting disease disease resistance Disease Susceptibility - veterinary disease transmission Encephalopathy, Bovine Spongiform - genetics epidemiology Fundamental and applied biological sciences. Psychology genes genetic polymorphism Genetic Predisposition to Disease genetic resistance Genotype Genotype & phenotype molecular sequence data Polymorphism Polymorphism, Genetic prion diseases Prion Diseases - genetics Prions Prions - genetics promoter regions Promoter Regions, Genetic scrapie Species Specificity Spongiform encephalopathies Terrestrial animal productions transmissible mink encephalopathy Vertebrates |
title | Polymorphisms of the prion gene promoter region that influence classical bovine spongiform encephalopathy susceptibility are not applicable to other transmissible spongiform encephalopathies in cattle |
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