中华传染病杂志
中華傳染病雜誌
중화전염병잡지
CHINESE JOURNAL OF INFECTIOUS DISEASES
2008年
5期
287-291
,共5页
谢新宝%朱启镕%陈素清%缪金剑%王晓红
謝新寶%硃啟镕%陳素清%繆金劍%王曉紅
사신보%주계용%진소청%무금검%왕효홍
免疫球蛋白类%肝炎病毒,乙型%前C区变异%启动区(遗传学)%变异(遗传学)%疾病传播,垂直
免疫毬蛋白類%肝炎病毒,乙型%前C區變異%啟動區(遺傳學)%變異(遺傳學)%疾病傳播,垂直
면역구단백류%간염병독,을형%전C구변이%계동구(유전학)%변이(유전학)%질병전파,수직
Immunoglobulins%Hepatitis B virus%Precore mutantion%Promoter regions (genetics)%Variation (genetics)%Disease transmission,vertical
目的 探讨产前阻断,即产前注射乙型肝炎免疫球蛋白(HBIG)对HBV前C区和基本C启动子(BCP)区核苷酸序列的影响.方法 无症状慢性HBV携带孕妇120例,产前阻断HBIG组67例,不产前阻断非HBIG组53例,荧光定量PCR法检测血清HBV DNA载量,ELISA检测血清HBsAg、HBeAg,套式PCR扩增HBV DNA前C区和BCP区核苷酸片段,DNA自动荧光测序仪对PCR产物直接测序.组间均数比较采用t检验,组间率比较采用卡方检验.结果 HBIG组33例孕妇收集到阻断前、后双份血清,其中23例阻断前、后HBV DNA前c区、BCP区均扩增测序成功.阻断前、后HBV前C区+BCP区、前C区、BCP区核苷酸的替代变异率分别为1.5%和1.4%、0.7%和0.6%、1.7%和1.7%(Fisher's精确检验,x2值分别为0.627、0.689、1.000,P＞0.05).阻断前、后1896G→A、1899G→A、1762A→T、1764G→A热点总变异发生率分别为27.2%和13.0%(x2=5.717,P=0.017),但各热点变异的发生率阻断前、后分别为30.4%和17.4%、17.4%和4.3%、26.1%和13.0%、34.8%和17.4%,差异无统计学意义(P＞0.05).扩增成功的53例HBIG组和47例非HBIG组孕妇临产时HBV DNA前C区+BCP区、前C区、BCP区核苷酸的替代变异率分别为0.9%和0.8%、0.3%和0.3%、1.1%和0.9%(Fisher's精确检验,x2值分别为0.434、0.839、0.340,P＞0.05);HBIG组和非HBIG组孕妇1896G→A、1899G→A、1762A→T、1764G→A热点总变异发生率及各热点变异发生率分别为5.7%和10.1%、9.4%和14.9%、0和2.1%、7.5%和10.6%、5.7%和12.8%,但差异无统计学意义(P＞0.05).结论 产前阻断可能不增加孕妇HBV DNA前C区、BCP区核苷酸变异;产前阻断可能减少孕妇体内HBV前C区、BCP区热点变异的发生.
目的 探討產前阻斷,即產前註射乙型肝炎免疫毬蛋白(HBIG)對HBV前C區和基本C啟動子(BCP)區覈苷痠序列的影響.方法 無癥狀慢性HBV攜帶孕婦120例,產前阻斷HBIG組67例,不產前阻斷非HBIG組53例,熒光定量PCR法檢測血清HBV DNA載量,ELISA檢測血清HBsAg、HBeAg,套式PCR擴增HBV DNA前C區和BCP區覈苷痠片段,DNA自動熒光測序儀對PCR產物直接測序.組間均數比較採用t檢驗,組間率比較採用卡方檢驗.結果 HBIG組33例孕婦收集到阻斷前、後雙份血清,其中23例阻斷前、後HBV DNA前c區、BCP區均擴增測序成功.阻斷前、後HBV前C區+BCP區、前C區、BCP區覈苷痠的替代變異率分彆為1.5%和1.4%、0.7%和0.6%、1.7%和1.7%(Fisher's精確檢驗,x2值分彆為0.627、0.689、1.000,P＞0.05).阻斷前、後1896G→A、1899G→A、1762A→T、1764G→A熱點總變異髮生率分彆為27.2%和13.0%(x2=5.717,P=0.017),但各熱點變異的髮生率阻斷前、後分彆為30.4%和17.4%、17.4%和4.3%、26.1%和13.0%、34.8%和17.4%,差異無統計學意義(P＞0.05).擴增成功的53例HBIG組和47例非HBIG組孕婦臨產時HBV DNA前C區+BCP區、前C區、BCP區覈苷痠的替代變異率分彆為0.9%和0.8%、0.3%和0.3%、1.1%和0.9%(Fisher's精確檢驗,x2值分彆為0.434、0.839、0.340,P＞0.05);HBIG組和非HBIG組孕婦1896G→A、1899G→A、1762A→T、1764G→A熱點總變異髮生率及各熱點變異髮生率分彆為5.7%和10.1%、9.4%和14.9%、0和2.1%、7.5%和10.6%、5.7%和12.8%,但差異無統計學意義(P＞0.05).結論 產前阻斷可能不增加孕婦HBV DNA前C區、BCP區覈苷痠變異;產前阻斷可能減少孕婦體內HBV前C區、BCP區熱點變異的髮生.
목적 탐토산전조단,즉산전주사을형간염면역구단백(HBIG)대HBV전C구화기본C계동자(BCP)구핵감산서렬적영향.방법 무증상만성HBV휴대잉부120례,산전조단HBIG조67례,불산전조단비HBIG조53례,형광정량PCR법검측혈청HBV DNA재량,ELISA검측혈청HBsAg、HBeAg,투식PCR확증HBV DNA전C구화BCP구핵감산편단,DNA자동형광측서의대PCR산물직접측서.조간균수비교채용t검험,조간솔비교채용잡방검험.결과 HBIG조33례잉부수집도조단전、후쌍빈혈청,기중23례조단전、후HBV DNA전c구、BCP구균확증측서성공.조단전、후HBV전C구+BCP구、전C구、BCP구핵감산적체대변이솔분별위1.5%화1.4%、0.7%화0.6%、1.7%화1.7%(Fisher's정학검험,x2치분별위0.627、0.689、1.000,P＞0.05).조단전、후1896G→A、1899G→A、1762A→T、1764G→A열점총변이발생솔분별위27.2%화13.0%(x2=5.717,P=0.017),단각열점변이적발생솔조단전、후분별위30.4%화17.4%、17.4%화4.3%、26.1%화13.0%、34.8%화17.4%,차이무통계학의의(P＞0.05).확증성공적53례HBIG조화47례비HBIG조잉부임산시HBV DNA전C구+BCP구、전C구、BCP구핵감산적체대변이솔분별위0.9%화0.8%、0.3%화0.3%、1.1%화0.9%(Fisher's정학검험,x2치분별위0.434、0.839、0.340,P＞0.05);HBIG조화비HBIG조잉부1896G→A、1899G→A、1762A→T、1764G→A열점총변이발생솔급각열점변이발생솔분별위5.7%화10.1%、9.4%화14.9%、0화2.1%、7.5%화10.6%、5.7%화12.8%,단차이무통계학의의(P＞0.05).결론 산전조단가능불증가잉부HBV DNA전C구、BCP구핵감산변이;산전조단가능감소잉부체내HBV전C구、BCP구열점변이적발생.
Objective To investigate the impact of injecting hepatitis B immune globulin(HBIG)at third trimester of pregnancy on the nucleotide sequences of precore and basal core promoter(BCP)regions of hepatitis B virus(HBV)DNA.Methods One hundred and twenty pregnant women(67 in HBIG group and 53 in no-HBIG group)were enrolled in this study.Serum HBV DNA level was determined using quantitative real-time polymerase chain reaction(RT-PCR).Relevant serum markers (HBeAg,HBsAg)of HBV were detected by enzyme-linked immunosorbent assay(ELISA).Nucleotide fragments of HBV precore and BCP regions were amplified by nested PCR and then sequenced by automated DNA sequencer.Data were analyzed using t test and chi-square test.Results Sera of 33 women in HBIG group were collected before interruption with HBIG and at delivery.Precore and BCP regions of HBV DNA were amplified and sequenced successfully from double sera of 23 among 33 women. The rates of total nucleotide substitute in precore and BCP regions, that in precore region, and that in BCP region before and after interruption were 1.5% and 1.4%, 0.7% and 0.6%, 1.7% and 1.7%, respectively (Fisher's exact test, X2 =0.627, 0.689, 1.000, respectively,all P＞0.05). The rates of total mutations of hot points including 1896G→A,1899G→A,1762A→T,1764G→A before and after interruption were 27.2% and 13.0%, respectively (x2=5.717, P=0. 017). But the prevalences of these hot points mutations before and after interruption were 30.4%and 17.4%, 17.40/00 and 4.3%, 26.1% and 13.0%, 34.80/00 and 17.4%, respectively, which were all not significantly different (P＞0.05). The rates of nucleotide substitute in precore and BCP regions,that in precore region, and that in BCP region of 53 women in HBIG group and 47 women in no-HBIG group at delivery were 0.9% and 0.8%, 0.3% and 0.3%, 1.1% and 0.9%, respectively (Fisher's exact test, )x2=0.434, 0.839, 0.340, respectively, all P＞0. 05). The rates of total mutations of hot points of women in HBIG group and those in no-HBIG group at delivery were 5.7% and 10.1%,respectively, which was not significantly different (P＞0.05). These hot points mutations including 1896G→A,1899G→A,1762A→T, 1764G→A of women in HBIG group and those in no-HBIG group at delivery were 9.4% and 14.9%, 0 and 2. 1%, 7.5%0 and 10.6%, 5.7% and 12.8%, respectively,which were all not significantly different ( P＞0.05). Conclusions Antepartum interruption of HBV intrauterine infection with HBIG may not raise the nucleotide mutations in precore and BCP regions of HBV DNA. On the other hand, antepartum interruption may decrease mutations of hot points in the precore and BCP regions of HBV DNA.
