Influences of MxA gene –88 G/T and IFN‐gamma +874 A/T on the natural history of hepatitis B virus infection in an endemic area
Identifieur interne : 000977 ( Istex/Corpus ); précédent : 000976; suivant : 000978Influences of MxA gene –88 G/T and IFN‐gamma +874 A/T on the natural history of hepatitis B virus infection in an endemic area
Auteurs : X. M. Peng ; R. X. Lei ; L. Gu ; H. H. Ma ; Q. F. Xie ; Z. L. GaoSource :
- International Journal of Immunogenetics [ 1744-3121 ] ; 2007-10.
Abstract
The influence of human genetics on the natural history of hepatitis B virus (HBV) infection may be diminished in endemic areas because infection at a young age predisposes to chronic HBV infection. The present study aimed to address this issue through the determination of the influences of single nucleotide polymorphisms (SNPs) of myxovirus resistence‐1 (MxA) –88 G/T and interferon (IFN)‐gamma +874 A/T on the natural history of HBV infection in endemic regions. One hundred adult patients with self‐limiting HBV infection (positive for both anti‐HBs and anti‐HBc) and 340 adult patients with persistent HBV infection were recruited from southern China, an endemic area with an HBsAg carrier rate of 17.8%. SNPs of MxA –88 G/T and interferon (IFN)‐gamma +874 A/T were typed using a protocol based on competitively differentiated polymerase chain reaction. A highly significant difference in the distribution of MxA –88 G/T was observed between those with persistent and self‐limiting HBV infections. The latter displayed a lower frequency of the GG genotype (41.0% vs. 52.9%, P = 0.036) and a higher frequency of the TT genotype (16.0% vs. 2.4%, P = 0.000), compared to patients with persistent infection. These differences were not gender‐ or age‐specific. However, a significant distribution difference of IFN‐gamma +874 A/T was not observed. Between two groups of patients, respectively, the distribution frequencies of the AA genotype (65.0% vs. 72.8%, P = 0.139) and the TT genotype (2.0% vs. 1.2%, P = 0.894) were found. These results suggest that MxA gene –88 G/T and IFN‐gamma +874 A/T behave differently in endemic HBV infections. Further study is necessary to clarify the influences of human genetics on endemic HBV infections.
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DOI: 10.1111/j.1744-313X.2007.00696.x
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Lei</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation></author><author><name sortKey="Gu, L" sort="Gu, L" uniqKey="Gu L" first="L." last="Gu">L. Gu</name><affiliation><mods:affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</mods:affiliation></affiliation></author><author><name sortKey="Ma, H H" sort="Ma, H H" uniqKey="Ma H" first="H. H." last="Ma">H. H. Ma</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation></author><author><name sortKey="Xie, Q F" sort="Xie, Q F" uniqKey="Xie Q" first="Q. F." last="Xie">Q. F. Xie</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation><affiliation><mods:affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</mods:affiliation></affiliation></author><author><name sortKey="Gao, Z L" sort="Gao, Z L" uniqKey="Gao Z" first="Z. L." last="Gao">Z. L. 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M." last="Peng">X. M. Peng</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation><affiliation><mods:affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</mods:affiliation></affiliation></author><author><name sortKey="Lei, R X" sort="Lei, R X" uniqKey="Lei R" first="R. X." last="Lei">R. X. Lei</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation></author><author><name sortKey="Gu, L" sort="Gu, L" uniqKey="Gu L" first="L." last="Gu">L. Gu</name><affiliation><mods:affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</mods:affiliation></affiliation></author><author><name sortKey="Ma, H H" sort="Ma, H H" uniqKey="Ma H" first="H. H." last="Ma">H. H. Ma</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation></author><author><name sortKey="Xie, Q F" sort="Xie, Q F" uniqKey="Xie Q" first="Q. F." last="Xie">Q. F. Xie</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation><affiliation><mods:affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</mods:affiliation></affiliation></author><author><name sortKey="Gao, Z L" sort="Gao, Z L" uniqKey="Gao Z" first="Z. L." last="Gao">Z. L. Gao</name><affiliation><mods:affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</mods:affiliation></affiliation><affiliation><mods:affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">International Journal of Immunogenetics</title><title level="j" type="alt">INTERNATIONAL JOURNAL OF IMMUNOGENETICS</title><idno type="ISSN">1744-3121</idno><idno type="eISSN">1744-313X</idno><imprint><biblScope unit="vol">34</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="341">341</biblScope><biblScope unit="page" to="346">346</biblScope><biblScope unit="page-count">6</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2007-10">2007-10</date></imprint><idno type="ISSN">1744-3121</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1744-3121</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The influence of human genetics on the natural history of hepatitis B virus (HBV) infection may be diminished in endemic areas because infection at a young age predisposes to chronic HBV infection. The present study aimed to address this issue through the determination of the influences of single nucleotide polymorphisms (SNPs) of myxovirus resistence‐1 (MxA) –88 G/T and interferon (IFN)‐gamma +874 A/T on the natural history of HBV infection in endemic regions. One hundred adult patients with self‐limiting HBV infection (positive for both anti‐HBs and anti‐HBc) and 340 adult patients with persistent HBV infection were recruited from southern China, an endemic area with an HBsAg carrier rate of 17.8%. SNPs of MxA –88 G/T and interferon (IFN)‐gamma +874 A/T were typed using a protocol based on competitively differentiated polymerase chain reaction. A highly significant difference in the distribution of MxA –88 G/T was observed between those with persistent and self‐limiting HBV infections. The latter displayed a lower frequency of the GG genotype (41.0% vs. 52.9%, P = 0.036) and a higher frequency of the TT genotype (16.0% vs. 2.4%, P = 0.000), compared to patients with persistent infection. These differences were not gender‐ or age‐specific. However, a significant distribution difference of IFN‐gamma +874 A/T was not observed. Between two groups of patients, respectively, the distribution frequencies of the AA genotype (65.0% vs. 72.8%, P = 0.139) and the TT genotype (2.0% vs. 1.2%, P = 0.894) were found. These results suggest that MxA gene –88 G/T and IFN‐gamma +874 A/T behave differently in endemic HBV infections. 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The present study aimed to address this issue through the determination of the influences of single nucleotide polymorphisms (SNPs) of myxovirus resistence‐1 (MxA) –88 G/T and interferon (IFN)‐gamma +874 A/T on the natural history of HBV infection in endemic regions. One hundred adult patients with self‐limiting HBV infection (positive for both anti‐HBs and anti‐HBc) and 340 adult patients with persistent HBV infection were recruited from southern China, an endemic area with an HBsAg carrier rate of 17.8%. SNPs of MxA –88 G/T and interferon (IFN)‐gamma +874 A/T were typed using a protocol based on competitively differentiated polymerase chain reaction. A highly significant difference in the distribution of MxA –88 G/T was observed between those with persistent and self‐limiting HBV infections. The latter displayed a lower frequency of the GG genotype (41.0% vs. 52.9%, P = 0.036) and a higher frequency of the TT genotype (16.0% vs. 2.4%, P = 0.000), compared to patients with persistent infection. These differences were not gender‐ or age‐specific. However, a significant distribution difference of IFN‐gamma +874 A/T was not observed. Between two groups of patients, respectively, the distribution frequencies of the AA genotype (65.0% vs. 72.8%, P = 0.139) and the TT genotype (2.0% vs. 1.2%, P = 0.894) were found. These results suggest that MxA gene –88 G/T and IFN‐gamma +874 A/T behave differently in endemic HBV infections. Further study is necessary to clarify the influences of human genetics on endemic HBV infections.</abstract><qualityIndicators><score>8.538</score><pdfWordCount>3538</pdfWordCount><pdfCharCount>23057</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>595 x 788 pts</pdfPageSize><pdfWordsPerPage>590</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>259</abstractWordCount><abstractCharCount>1740</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Influences of MxA gene –88 G/T and IFN‐gamma +874 A/T on the natural history of hepatitis B virus infection in an endemic area</title><pmid><json:string>17845304</json:string></pmid><genre><json:string>article</json:string></genre><host><title>International Journal of Immunogenetics</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1744-313X</json:string></doi><issn><json:string>1744-3121</json:string></issn><eissn><json:string>1744-313X</json:string></eissn><publisherId><json:string>IJI</json:string></publisherId><volume>34</volume><issue>5</issue><pages><first>341</first><last>346</last><total>6</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2007</json:string></date><geogName></geogName><orgName><json:string>Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China</json:string><json:string>Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China Received</json:string><json:string>Roche Diagnostic Ltd</json:string><json:string>Hospital, Sun Yat-Sen University</json:string><json:string>Blackwell Publishing Ltd, International Journal</json:string><json:string>Department of Infectious Diseases</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Z. L. Gao</json:string><json:string>Hong Kong</json:string><json:string>H. H. Ma</json:string><json:string>Q. F. Xie</json:string><json:string>G. Li</json:string><json:string>L. Gu</json:string><json:string>C. L. Yao</json:string><json:string>Xiao Mou</json:string><json:string>R. X. Lei</json:string></persName><placeName><json:string>IL</json:string><json:string>China</json:string><json:string>USA</json:string><json:string>Chicago</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Fernandez-Arcas et al., 2004</json:string><json:string>Yao, 1996</json:string><json:string>Biron et al., 1999</json:string><json:string>Chong et al., 2006</json:string><json:string>Ben-Ari et al., 2003</json:string><json:string>X. M. 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M.</forename><surname>Peng</surname></persName><affiliation><orgName type="division"> Department of Infectious Diseases</orgName><orgName type="institution">Third Affiliated Hospital</orgName><orgName type="institution">Sun Yat‐Sen University</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China and</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation><affiliation><orgName type="institution"> Clinical and Experimental Research Center of Viral Hepatitis</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">R. X.</forename><surname>Lei</surname></persName><affiliation><orgName type="division"> Department of Infectious Diseases</orgName><orgName type="institution">Third Affiliated Hospital</orgName><orgName type="institution">Sun Yat‐Sen University</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China and</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">L.</forename><surname>Gu</surname></persName><affiliation><orgName type="institution"> Clinical and Experimental Research Center of Viral Hepatitis</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">H. H.</forename><surname>Ma</surname></persName><affiliation><orgName type="division"> Department of Infectious Diseases</orgName><orgName type="institution">Third Affiliated Hospital</orgName><orgName type="institution">Sun Yat‐Sen University</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China and</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Q. F.</forename><surname>Xie</surname></persName><affiliation><orgName type="division"> Department of Infectious Diseases</orgName><orgName type="institution">Third Affiliated Hospital</orgName><orgName type="institution">Sun Yat‐Sen University</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China and</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation><affiliation><orgName type="institution"> Clinical and Experimental Research Center of Viral Hepatitis</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Z. L.</forename><surname>Gao</surname></persName><affiliation><orgName type="division"> Department of Infectious Diseases</orgName><orgName type="institution">Third Affiliated Hospital</orgName><orgName type="institution">Sun Yat‐Sen University</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China and</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation><affiliation><orgName type="institution"> Clinical and Experimental Research Center of Viral Hepatitis</orgName><address><addrLine>Guangzhou</addrLine><addrLine>Guangdong, China</addrLine><country key="CN" xml:lang="en">CHINA</country></address></affiliation></author><idno type="istex">1082DDB509EC63A6537696203BC502CBE1CFB517</idno><idno type="ark">ark:/67375/WNG-BC0DVGCC-5</idno><idno type="DOI">10.1111/j.1744-313X.2007.00696.x</idno><idno type="unit">IJI696</idno><idno type="toTypesetVersion">file:IJI.IJI696.pdf</idno></analytic><monogr><title level="j" type="main">International Journal of Immunogenetics</title><title level="j" type="alt">INTERNATIONAL JOURNAL OF IMMUNOGENETICS</title><idno type="pISSN">1744-3121</idno><idno type="eISSN">1744-313X</idno><idno type="book-DOI">10.1111/(ISSN)1744-313X</idno><idno type="book-part-DOI">10.1111/eji.2007.34.issue-5</idno><idno type="product">IJI</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">34</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="341">341</biblScope><biblScope unit="page" to="346">346</biblScope><biblScope unit="page-count">6</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2007-10"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><head>Summary</head><p>The influence of human genetics on the natural history of hepatitis B virus (HBV) infection may be diminished in endemic areas because infection at a young age predisposes to chronic HBV infection. The present study aimed to address this issue through the determination of the influences of single nucleotide polymorphisms (SNPs) of myxovirus resistence‐1 (MxA) –88 G/T and interferon (IFN)‐gamma +874 A/T on the natural history of HBV infection in endemic regions.</p><p>One hundred adult patients with self‐limiting HBV infection (positive for both anti‐HBs and anti‐HBc) and 340 adult patients with persistent HBV infection were recruited from southern China, an endemic area with an HBsAg carrier rate of 17.8%. SNPs of MxA –88 G/T and interferon (IFN)‐gamma +874 A/T were typed using a protocol based on competitively differentiated polymerase chain reaction. A highly significant difference in the distribution of MxA –88 G/T was observed between those with persistent and self‐limiting HBV infections. The latter displayed a lower frequency of the GG genotype (41.0% vs. 52.9%, <hi rend="italic">P</hi> = 0.036) and a higher frequency of the TT genotype (16.0% vs. 2.4%, <hi rend="italic">P</hi> = 0.000), compared to patients with persistent infection. These differences were not gender‐ or age‐specific. However, a significant distribution difference of IFN‐gamma +874 A/T was not observed. Between two groups of patients, respectively, the distribution frequencies of the AA genotype (65.0% vs. 72.8%, <hi rend="italic">P</hi> = 0.139) and the TT genotype (2.0% vs. 1.2%, <hi rend="italic">P</hi> = 0.894) were found. These results suggest that MxA gene –88 G/T and IFN‐gamma +874 A/T behave differently in endemic HBV infections. Further study is necessary to clarify the influences of human genetics on endemic HBV infections.</p></abstract><textClass><keywords rend="tocHeading1"><term>Original Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-BC0DVGCC-5/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)1744-313X</doi><issn type="print">1744-3121</issn><issn type="electronic">1744-313X</issn><idGroup><id type="product" value="IJI"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="INTERNATIONAL JOURNAL OF IMMUNOGENETICS">International Journal of Immunogenetics</title></titleGroup></publicationMeta><publicationMeta level="part" position="10005"><doi origin="wiley">10.1111/eji.2007.34.issue-5</doi><numberingGroup><numbering type="journalVolume" number="34">34</numbering><numbering type="journalIssue" number="5">5</numbering></numberingGroup><coverDate startDate="2007-10">October 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="6" status="forIssue"><doi origin="wiley">10.1111/j.1744-313X.2007.00696.x</doi><idGroup><id type="unit" value="IJI696"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2007-06-08"></event><event type="publishedOnlineFinalForm" date="2007-06-18"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-28"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-23"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="341">341</numbering><numbering type="pageLast" number="346">346</numbering></numberingGroup><correspondenceTo> Prof Xiao Mou Peng, Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, 600 Tianhe Road, Guangzhou 510630, China. Tel: +86 20 8759 0617; Fax: +86 20 8758 4302; E‐mail: <email>xiaomoupeng@hotmail.com</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:IJI.IJI696.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 17 April 2007; revised 17 April 2007; accepted 17 May 2007</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="4"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="25"></count><count type="wordTotal" number="3111"></count></countGroup><titleGroup><title type="main">Influences of MxA gene –88 G/T and IFN‐gamma +874 A/T on the natural history of hepatitis B virus infection in an endemic area</title><title type="shortAuthors">X. M. Peng <i>et al.</i></title><title type="short">Gene SNPs and endemic HBV infection</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>X. M.</givenNames><familyName>Peng</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>R. X.</givenNames><familyName>Lei</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>L.</givenNames><familyName>Gu</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>H. H.</givenNames><familyName>Ma</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1 #a2"><personName><givenNames>Q. F.</givenNames><familyName>Xie</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1 #a2"><personName><givenNames>Z. L.</givenNames><familyName>Gao</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CN"><unparsedAffiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CN"><unparsedAffiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Summary</title><p>The influence of human genetics on the natural history of hepatitis B virus (HBV) infection may be diminished in endemic areas because infection at a young age predisposes to chronic HBV infection. The present study aimed to address this issue through the determination of the influences of single nucleotide polymorphisms (SNPs) of myxovirus resistence‐1 (MxA) –88 G/T and interferon (IFN)‐gamma +874 A/T on the natural history of HBV infection in endemic regions.</p><p>One hundred adult patients with self‐limiting HBV infection (positive for both anti‐HBs and anti‐HBc) and 340 adult patients with persistent HBV infection were recruited from southern China, an endemic area with an HBsAg carrier rate of 17.8%. SNPs of MxA –88 G/T and interferon (IFN)‐gamma +874 A/T were typed using a protocol based on competitively differentiated polymerase chain reaction. A highly significant difference in the distribution of MxA –88 G/T was observed between those with persistent and self‐limiting HBV infections. The latter displayed a lower frequency of the GG genotype (41.0% vs. 52.9%, <i>P</i> = 0.036) and a higher frequency of the TT genotype (16.0% vs. 2.4%, <i>P</i> = 0.000), compared to patients with persistent infection. These differences were not gender‐ or age‐specific. However, a significant distribution difference of IFN‐gamma +874 A/T was not observed. Between two groups of patients, respectively, the distribution frequencies of the AA genotype (65.0% vs. 72.8%, <i>P</i> = 0.139) and the TT genotype (2.0% vs. 1.2%, <i>P</i> = 0.894) were found. These results suggest that MxA gene –88 G/T and IFN‐gamma +874 A/T behave differently in endemic HBV infections. Further study is necessary to clarify the influences of human genetics on endemic HBV infections.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Influences of MxA gene –88 G/T and IFN‐gamma +874 A/T on the natural history of hepatitis B virus infection in an endemic area</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Gene SNPs and endemic HBV infection</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Influences of MxA gene –88 G/T and IFN‐gamma +874 A/T on the natural history of hepatitis B virus infection in an endemic area</title></titleInfo><name type="personal"><namePart type="given">X. M.</namePart><namePart type="family">Peng</namePart><affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</affiliation><affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R. X.</namePart><namePart type="family">Lei</namePart><affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Gu</namePart><affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H. H.</namePart><namePart type="family">Ma</namePart><affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Q. F.</namePart><namePart type="family">Xie</namePart><affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</affiliation><affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Z. L.</namePart><namePart type="family">Gao</namePart><affiliation> Department of Infectious Diseases, Third Affiliated Hospital, Sun Yat‐Sen University, Guangzhou, Guangdong, China and</affiliation><affiliation> Clinical and Experimental Research Center of Viral Hepatitis, Guangzhou, Guangdong, China</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">2007-10</dateIssued><edition>Received 17 April 2007; revised 17 April 2007; accepted 17 May 2007</edition><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">1</extent><extent unit="tables">4</extent><extent unit="formulas">0</extent><extent unit="references">25</extent><extent unit="words">3111</extent></physicalDescription><abstract lang="en">The influence of human genetics on the natural history of hepatitis B virus (HBV) infection may be diminished in endemic areas because infection at a young age predisposes to chronic HBV infection. The present study aimed to address this issue through the determination of the influences of single nucleotide polymorphisms (SNPs) of myxovirus resistence‐1 (MxA) –88 G/T and interferon (IFN)‐gamma +874 A/T on the natural history of HBV infection in endemic regions. One hundred adult patients with self‐limiting HBV infection (positive for both anti‐HBs and anti‐HBc) and 340 adult patients with persistent HBV infection were recruited from southern China, an endemic area with an HBsAg carrier rate of 17.8%. SNPs of MxA –88 G/T and interferon (IFN)‐gamma +874 A/T were typed using a protocol based on competitively differentiated polymerase chain reaction. A highly significant difference in the distribution of MxA –88 G/T was observed between those with persistent and self‐limiting HBV infections. The latter displayed a lower frequency of the GG genotype (41.0% vs. 52.9%, P = 0.036) and a higher frequency of the TT genotype (16.0% vs. 2.4%, P = 0.000), compared to patients with persistent infection. These differences were not gender‐ or age‐specific. However, a significant distribution difference of IFN‐gamma +874 A/T was not observed. Between two groups of patients, respectively, the distribution frequencies of the AA genotype (65.0% vs. 72.8%, P = 0.139) and the TT genotype (2.0% vs. 1.2%, P = 0.894) were found. These results suggest that MxA gene –88 G/T and IFN‐gamma +874 A/T behave differently in endemic HBV infections. Further study is necessary to clarify the influences of human genetics on endemic HBV infections.</abstract><relatedItem type="host"><titleInfo><title>International Journal of Immunogenetics</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">1744-3121</identifier><identifier type="eISSN">1744-313X</identifier><identifier type="DOI">10.1111/(ISSN)1744-313X</identifier><identifier type="PublisherID">IJI</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>34</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>341</start><end>346</end><total>6</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>The current status of antiviral therapy of chronic hepatitis B</title></titleInfo><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Asselah</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.P.</namePart><namePart type="family">Ripault</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Castelnau</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Giuily</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N.</namePart><namePart type="family">Boyer</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Marcellin</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Asselah, T., Ripault, M.P., Castelnau, C., Giuily, N., Boyer, N. & Marcellin, P. 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