Molecular and serological characterization of hepatitis B virus in deferred Ghanaian blood donors with and without elevated alanine aminotransferase
Identifieur interne : 004096 ( Istex/Corpus ); précédent : 004095; suivant : 004097Molecular and serological characterization of hepatitis B virus in deferred Ghanaian blood donors with and without elevated alanine aminotransferase
Auteurs : D. Candotti ; O. Opare-Sem ; H. Rezvan ; F. Sarkodie ; J. AllainSource :
- Journal of Viral Hepatitis [ 1352-0504 ] ; 2006-11.
English descriptors
- KwdEn :
- Alanine, Alanine aminotransferase, Aminotransferase, Antigen seroconversion, Assay, Asymptomatic, Authors journal compilation, Basic core promoter, Blackwell publishing, Blood donors, Bootstrap values, Candidate blood donors, Candotti, Chronic carriage, Chronic hepatitis, Clin microbiol, Core promoter, Direct sequencing, Donor, Double mutation, Gene sequences, Genetic diversity, Genotype, Ghanaian, Ghanaian blood donors, Ghanaian sequences, Hbeag, Hbeag positivity, Hbeag prevalence, Hepatitis, Hepatocellular carcinoma, High frequency, High prevalence, Identical sequences, Line probe assay, Liver disease, Median, Mutant, Mutation, Natural history, Nucleotide, Precore, Present study, Promoter, Reference sequences, Replication, Risk factors, Sequencing, Seroconversion, Surface antigen, Viral, Viral hepatitis, Viral load, Viral replication, Virol, Virus genotype, West africa.
- Teeft :
- Alanine, Alanine aminotransferase, Aminotransferase, Antigen seroconversion, Assay, Asymptomatic, Authors journal compilation, Basic core promoter, Blackwell publishing, Blood donors, Bootstrap values, Candidate blood donors, Candotti, Chronic carriage, Chronic hepatitis, Clin microbiol, Core promoter, Direct sequencing, Donor, Double mutation, Gene sequences, Genetic diversity, Genotype, Ghanaian, Ghanaian blood donors, Ghanaian sequences, Hbeag, Hbeag positivity, Hbeag prevalence, Hepatitis, Hepatocellular carcinoma, High frequency, High prevalence, Identical sequences, Line probe assay, Liver disease, Median, Mutant, Mutation, Natural history, Nucleotide, Precore, Present study, Promoter, Reference sequences, Replication, Risk factors, Sequencing, Seroconversion, Surface antigen, Viral, Viral hepatitis, Viral load, Viral replication, Virol, Virus genotype, West africa.
Abstract
Summary. Candidate blood donors in Ghana are frequent carriers of hepatitis B virus (HBV). A comparative study of 117 donor samples including 46 with alanine aminotransferase (ALT) ≥ 60 IU/L and 71 with ≤40 IU/L level was undertaken. S and the basic core promoter‐precore regions (BCP/PC) sequencing was used to identify genotypes and variants relevant to HBV natural history, respectively. Age, viral load, HBe status were correlated with molecular data. HBV genotype E (87%) was dominant with little genotypes A (10%) and D (3%). Comparing individuals with or without liver disease, an association between liver disease and older age (P = 0.004) and higher viral load (P = 0.002) whether as a whole population or only genotype E was found. Compared with a commercial assay, BCP/PC sequencing had lower sensitivity to detect mixtures of wild‐type and variant viruses but detected BCP deletions. BCP 1762/1764 variants were positively correlated with older age (P < 0.0001) and elevated ALT levels (P = 0.01). PC 1896 stop codon was marginally correlated with viral load (P = 0.09). HBV genotype E infection natural history appears different from genotypes B and C prevalent in Asia. Donors with liver disease being older, with higher viral load and higher BCP variant proportion may be at higher risk of cirrhosis and hepatocellular carcinoma
Url:
DOI: 10.1111/j.1365-2893.2006.00741.x
Links to Exploration step
ISTEX:C7232A1DA839DD6912BF0F1CC4C3C600B543BD0BLe document en format XML
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Rezvan</name><affiliation><mods:affiliation>Iranian Blood Transfusion Organisation‐Research Centre, Tehran, Iran</mods:affiliation></affiliation></author><author><name sortKey="Sarkodie, F" sort="Sarkodie, F" uniqKey="Sarkodie F" first="F." last="Sarkodie">F. Sarkodie</name><affiliation><mods:affiliation>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana</mods:affiliation></affiliation></author><author><name sortKey="Allain, J" sort="Allain, J" uniqKey="Allain J" first="J." last="Allain">J. 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Candotti</name><affiliation><mods:affiliation>National Blood Service, Cambridge Blood Centre, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Opare Em, O" sort="Opare Em, O" uniqKey="Opare Em O" first="O." last="Opare-Sem">O. Opare-Sem</name><affiliation><mods:affiliation>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana</mods:affiliation></affiliation></author><author><name sortKey="Rezvan, H" sort="Rezvan, H" uniqKey="Rezvan H" first="H." last="Rezvan">H. Rezvan</name><affiliation><mods:affiliation>Iranian Blood Transfusion Organisation‐Research Centre, Tehran, Iran</mods:affiliation></affiliation></author><author><name sortKey="Sarkodie, F" sort="Sarkodie, F" uniqKey="Sarkodie F" first="F." last="Sarkodie">F. 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Candidate blood donors in Ghana are frequent carriers of hepatitis B virus (HBV). A comparative study of 117 donor samples including 46 with alanine aminotransferase (ALT) ≥ 60 IU/L and 71 with ≤40 IU/L level was undertaken. S and the basic core promoter‐precore regions (BCP/PC) sequencing was used to identify genotypes and variants relevant to HBV natural history, respectively. Age, viral load, HBe status were correlated with molecular data. HBV genotype E (87%) was dominant with little genotypes A (10%) and D (3%). Comparing individuals with or without liver disease, an association between liver disease and older age (P = 0.004) and higher viral load (P = 0.002) whether as a whole population or only genotype E was found. Compared with a commercial assay, BCP/PC sequencing had lower sensitivity to detect mixtures of wild‐type and variant viruses but detected BCP deletions. BCP 1762/1764 variants were positively correlated with older age (P < 0.0001) and elevated ALT levels (P = 0.01). PC 1896 stop codon was marginally correlated with viral load (P = 0.09). HBV genotype E infection natural history appears different from genotypes B and C prevalent in Asia. Donors with liver disease being older, with higher viral load and higher BCP variant proportion may be at higher risk of cirrhosis and hepatocellular carcinoma</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>genotype</json:string><json:string>viral</json:string><json:string>mutation</json:string><json:string>mutant</json:string><json:string>ghanaian</json:string><json:string>hbeag</json:string><json:string>precore</json:string><json:string>liver disease</json:string><json:string>sequencing</json:string><json:string>hepatitis</json:string><json:string>virol</json:string><json:string>viral load</json:string><json:string>seroconversion</json:string><json:string>direct sequencing</json:string><json:string>candotti</json:string><json:string>viral hepatitis</json:string><json:string>blackwell publishing</json:string><json:string>authors journal compilation</json:string><json:string>chronic hepatitis</json:string><json:string>aminotransferase</json:string><json:string>ghanaian blood donors</json:string><json:string>promoter</json:string><json:string>median</json:string><json:string>assay</json:string><json:string>asymptomatic</json:string><json:string>alanine</json:string><json:string>viral replication</json:string><json:string>replication</json:string><json:string>virus genotype</json:string><json:string>alanine aminotransferase</json:string><json:string>genetic diversity</json:string><json:string>hbeag prevalence</json:string><json:string>blood donors</json:string><json:string>west africa</json:string><json:string>core promoter</json:string><json:string>present study</json:string><json:string>donor</json:string><json:string>hbeag positivity</json:string><json:string>ghanaian sequences</json:string><json:string>risk factors</json:string><json:string>clin microbiol</json:string><json:string>identical sequences</json:string><json:string>hepatocellular carcinoma</json:string><json:string>reference sequences</json:string><json:string>natural history</json:string><json:string>surface antigen</json:string><json:string>candidate blood donors</json:string><json:string>double mutation</json:string><json:string>gene sequences</json:string><json:string>chronic carriage</json:string><json:string>line probe assay</json:string><json:string>basic core promoter</json:string><json:string>high frequency</json:string><json:string>antigen seroconversion</json:string><json:string>bootstrap values</json:string><json:string>high prevalence</json:string><json:string>nucleotide</json:string></teeft></keywords><author><json:item><name>D. Candotti</name><affiliations><json:string>National Blood Service, Cambridge Blood Centre, Cambridge, UK</json:string></affiliations></json:item><json:item><name>O. Opare‐Sem</name><affiliations><json:string>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana</json:string></affiliations></json:item><json:item><name>H. Rezvan</name><affiliations><json:string>Iranian Blood Transfusion Organisation‐Research Centre, Tehran, Iran</json:string></affiliations></json:item><json:item><name>F. Sarkodie</name><affiliations><json:string>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana</json:string></affiliations></json:item><json:item><name>J.‐P. Allain</name><affiliations><json:string>Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, UK</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>alanine aminotransferase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>blood donors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hepatitis B e antigen</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hepatitis B virus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>precore promoter</value></json:item></subject><articleId><json:string>JVH741</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Summary. Candidate blood donors in Ghana are frequent carriers of hepatitis B virus (HBV). A comparative study of 117 donor samples including 46 with alanine aminotransferase (ALT) ≥ 60 IU/L and 71 with ≤40 IU/L level was undertaken. S and the basic core promoter‐precore regions (BCP/PC) sequencing was used to identify genotypes and variants relevant to HBV natural history, respectively. Age, viral load, HBe status were correlated with molecular data. HBV genotype E (87%) was dominant with little genotypes A (10%) and D (3%). Comparing individuals with or without liver disease, an association between liver disease and older age (P = 0.004) and higher viral load (P = 0.002) whether as a whole population or only genotype E was found. Compared with a commercial assay, BCP/PC sequencing had lower sensitivity to detect mixtures of wild‐type and variant viruses but detected BCP deletions. BCP 1762/1764 variants were positively correlated with older age (P > 0.0001) and elevated ALT levels (P = 0.01). PC 1896 stop codon was marginally correlated with viral load (P = 0.09). HBV genotype E infection natural history appears different from genotypes B and C prevalent in Asia. Donors with liver disease being older, with higher viral load and higher BCP variant proportion may be at higher risk of cirrhosis and hepatocellular carcinoma</abstract><qualityIndicators><score>7.412</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1344</abstractCharCount><pdfWordCount>6514</pdfWordCount><pdfCharCount>40480</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>201</abstractWordCount></qualityIndicators><title>Molecular and serological characterization of hepatitis B virus in deferred Ghanaian blood donors with and without elevated alanine aminotransferase</title><genre><json:string>article</json:string></genre><host><title>Journal of Viral 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Cambridge Blood Centre, Cambridge, UK<address><country key="GB"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">O.</forename><surname>Opare‐Sem</surname></persName><affiliation>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana<address><country key="GH"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">H.</forename><surname>Rezvan</surname></persName><affiliation>Iranian Blood Transfusion Organisation‐Research Centre, Tehran, Iran</affiliation></author><author xml:id="author-0003"><persName><forename type="first">F.</forename><surname>Sarkodie</surname></persName><affiliation>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana<address><country key="GH"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">J.‐P.</forename><surname>Allain</surname></persName><affiliation>Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, UK<address><country key="GB"></country></address></affiliation></author><idno type="istex">C7232A1DA839DD6912BF0F1CC4C3C600B543BD0B</idno><idno type="ark">ark:/67375/WNG-HXX973SX-L</idno><idno type="DOI">10.1111/j.1365-2893.2006.00741.x</idno><idno type="unit">JVH741</idno><idno type="toTypesetVersion">file:JVH.JVH741.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Viral Hepatitis</title><title level="j" type="alt">JOURNAL OF VIRAL HEPATITIS</title><idno type="pISSN">1352-0504</idno><idno type="eISSN">1365-2893</idno><idno type="book-DOI">10.1111/(ISSN)1365-2893</idno><idno type="book-part-DOI">10.1111/jvh.2006.13.issue-11</idno><idno type="product">JVH</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">13</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="715">715</biblScope><biblScope unit="page" to="724">724</biblScope><biblScope unit="page-count">10</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-11"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Summary. </hi> Candidate blood donors in Ghana are frequent carriers of hepatitis B virus (HBV). A comparative study of 117 donor samples including 46 with alanine aminotransferase (ALT) ≥ 60 IU/L and 71 with ≤40 IU/L level was undertaken. S and the basic core promoter‐precore regions (BCP/PC) sequencing was used to identify genotypes and variants relevant to HBV natural history, respectively. Age, viral load, HBe status were correlated with molecular data. HBV genotype E (87%) was dominant with little genotypes A (10%) and D (3%). Comparing individuals with or without liver disease, an association between liver disease and older age (<hi rend="italic">P</hi> = 0.004) and higher viral load (<hi rend="italic">P</hi> = 0.002) whether as a whole population or only genotype E was found. Compared with a commercial assay, BCP/PC sequencing had lower sensitivity to detect mixtures of wild‐type and variant viruses but detected BCP deletions. BCP 1762/1764 variants were positively correlated with older age (<hi rend="italic">P</hi> < 0.0001) and elevated ALT levels (<hi rend="italic">P</hi> = 0.01). PC 1896 stop codon was marginally correlated with viral load (<hi rend="italic">P</hi> = 0.09). HBV genotype E infection natural history appears different from genotypes B and C prevalent in Asia. Donors with liver disease being older, with higher viral load and higher BCP variant proportion may be at higher risk of cirrhosis and hepatocellular carcinoma</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">alanine aminotransferase</term><term xml:id="k2">blood donors</term><term xml:id="k3">hepatitis B e antigen</term><term xml:id="k4">hepatitis B virus</term><term xml:id="k5">precore promoter</term></keywords><keywords rend="tocHeading1"><term>ORIGINAL ARTICLES</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/C7232A1DA839DD6912BF0F1CC4C3C600B543BD0B/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2893</doi><issn type="print">1352-0504</issn><issn type="electronic">1365-2893</issn><idGroup><id type="product" value="JVH"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF VIRAL HEPATITIS">Journal of Viral Hepatitis</title></titleGroup></publicationMeta><publicationMeta level="part" position="11011"><doi origin="wiley">10.1111/jvh.2006.13.issue-11</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue" number="11">11</numbering></numberingGroup><coverDate startDate="2006-11">November 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="1" status="forIssue"><doi origin="wiley">10.1111/j.1365-2893.2006.00741.x</doi><idGroup><id type="unit" value="JVH741"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title></titleGroup><eventGroup><event type="firstOnline" date="2006-06-26"></event><event type="publishedOnlineFinalForm" date="2006-06-26"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-01"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="715">715</numbering><numbering type="pageLast" number="724">724</numbering></numberingGroup><correspondenceTo>Dr Daniel Candotti, Cambridge Blood Centre, Long Road, Cambridge CB2 2PT, UK. E‐mail: <email>dc241@cam.ac.uk</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JVH.JVH741.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received May 2005; accepted for publication September 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="4"></count></countGroup><titleGroup><title type="main">Molecular and serological characterization of hepatitis B virus in deferred Ghanaian blood donors with and without elevated alanine aminotransferase</title><title type="shortAuthors"><i>D. Candotti</i> et al.</title><title type="short"><i>Hepatitis B infection in Ghanaian blood donors</i></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>D.</givenNames><familyName>Candotti</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>O.</givenNames><familyName>Opare‐Sem</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3"><personName><givenNames>H.</givenNames><familyName>Rezvan</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>F.</givenNames><familyName>Sarkodie</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a4"><personName><givenNames>J.‐P.</givenNames><familyName>Allain</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="GB"><unparsedAffiliation>National Blood Service, Cambridge Blood Centre, Cambridge, UK</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="GH"><unparsedAffiliation>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Iranian Blood Transfusion Organisation‐Research Centre, Tehran, Iran</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="GB"><unparsedAffiliation>Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, UK</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">alanine aminotransferase</keyword><keyword xml:id="k2">blood donors</keyword><keyword xml:id="k3">hepatitis B e antigen</keyword><keyword xml:id="k4">hepatitis B virus</keyword><keyword xml:id="k5">precore promoter</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Summary. </b> Candidate blood donors in Ghana are frequent carriers of hepatitis B virus (HBV). A comparative study of 117 donor samples including 46 with alanine aminotransferase (ALT) ≥ 60 IU/L and 71 with ≤40 IU/L level was undertaken. S and the basic core promoter‐precore regions (BCP/PC) sequencing was used to identify genotypes and variants relevant to HBV natural history, respectively. Age, viral load, HBe status were correlated with molecular data. HBV genotype E (87%) was dominant with little genotypes A (10%) and D (3%). Comparing individuals with or without liver disease, an association between liver disease and older age (<i>P</i> = 0.004) and higher viral load (<i>P</i> = 0.002) whether as a whole population or only genotype E was found. Compared with a commercial assay, BCP/PC sequencing had lower sensitivity to detect mixtures of wild‐type and variant viruses but detected BCP deletions. BCP 1762/1764 variants were positively correlated with older age (<i>P</i> < 0.0001) and elevated ALT levels (<i>P</i> = 0.01). PC 1896 stop codon was marginally correlated with viral load (<i>P</i> = 0.09). HBV genotype E infection natural history appears different from genotypes B and C prevalent in Asia. Donors with liver disease being older, with higher viral load and higher BCP variant proportion may be at higher risk of cirrhosis and hepatocellular carcinoma</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Molecular and serological characterization of hepatitis B virus in deferred Ghanaian blood donors with and without elevated alanine aminotransferase</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Hepatitis B infection in Ghanaian blood donors</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Molecular and serological characterization of hepatitis B virus in deferred Ghanaian blood donors with and without elevated alanine aminotransferase</title></titleInfo><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Candotti</namePart><affiliation>National Blood Service, Cambridge Blood Centre, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O.</namePart><namePart type="family">Opare‐Sem</namePart><affiliation>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Rezvan</namePart><affiliation>Iranian Blood Transfusion Organisation‐Research Centre, Tehran, Iran</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Sarkodie</namePart><affiliation>Department of Medicine, Komfo‐Anokye Teaching Hospital, Kumasi, Ghana</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.‐P.</namePart><namePart type="family">Allain</namePart><affiliation>Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-11</dateIssued><edition>Received May 2005; accepted for publication September 2005</edition><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">2</extent><extent unit="tables">4</extent></physicalDescription><abstract>Summary. Candidate blood donors in Ghana are frequent carriers of hepatitis B virus (HBV). A comparative study of 117 donor samples including 46 with alanine aminotransferase (ALT) ≥ 60 IU/L and 71 with ≤40 IU/L level was undertaken. S and the basic core promoter‐precore regions (BCP/PC) sequencing was used to identify genotypes and variants relevant to HBV natural history, respectively. Age, viral load, HBe status were correlated with molecular data. HBV genotype E (87%) was dominant with little genotypes A (10%) and D (3%). Comparing individuals with or without liver disease, an association between liver disease and older age (P = 0.004) and higher viral load (P = 0.002) whether as a whole population or only genotype E was found. Compared with a commercial assay, BCP/PC sequencing had lower sensitivity to detect mixtures of wild‐type and variant viruses but detected BCP deletions. BCP 1762/1764 variants were positively correlated with older age (P < 0.0001) and elevated ALT levels (P = 0.01). PC 1896 stop codon was marginally correlated with viral load (P = 0.09). HBV genotype E infection natural history appears different from genotypes B and C prevalent in Asia. Donors with liver disease being older, with higher viral load and higher BCP variant proportion may be at higher risk of cirrhosis and hepatocellular carcinoma</abstract><subject lang="en"><genre>keywords</genre><topic>alanine aminotransferase</topic><topic>blood donors</topic><topic>hepatitis B e antigen</topic><topic>hepatitis B virus</topic><topic>precore promoter</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Viral Hepatitis</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1352-0504</identifier><identifier type="eISSN">1365-2893</identifier><identifier type="DOI">10.1111/(ISSN)1365-2893</identifier><identifier type="PublisherID">JVH</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>715</start><end>724</end><total>10</total></extent></part></relatedItem><identifier type="istex">C7232A1DA839DD6912BF0F1CC4C3C600B543BD0B</identifier><identifier type="ark">ark:/67375/WNG-HXX973SX-L</identifier><identifier type="DOI">10.1111/j.1365-2893.2006.00741.x</identifier><identifier type="ArticleID">JVH741</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/C7232A1DA839DD6912BF0F1CC4C3C600B543BD0B/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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