中华传染病杂志
中華傳染病雜誌
중화전염병잡지
CHINESE JOURNAL OF INFECTIOUS DISEASES
2008年
3期
132-137
,共6页
郭丹华%王林%黄清玲%林万松%陈婉南%林旭
郭丹華%王林%黃清玲%林萬鬆%陳婉南%林旭
곽단화%왕림%황청령%림만송%진완남%림욱
肝炎病毒,乙型%基因缺失%基因组%突变%聚合酶链反应
肝炎病毒,乙型%基因缺失%基因組%突變%聚閤酶鏈反應
간염병독,을형%기인결실%기인조%돌변%취합매련반응
Hepatitis B virus%Gene deletion%Genome%Mutation%Polymerase chain reaction
目的 了解小分子HBV基因组缺失突变体的基因结构及特点.方法 采用一步法PCR从慢性乙型肝炎患者血清中扩增全基因组HBV DNA,回收并克隆＜1 kh的小分子HBV DNA,测序并以BioEdit及VectorNTI 6.0软件分析基因结构特点.结果 获得基因长度介于174～986 bp之间的64种、共124个小分子HBV缺失突变体DNA,按基因结构特点分为3类,即3种GT-AG剪接变异体、29种"常规"缺失突变体及32种基因组内部含polyA的缺失突变体.所有小分子基因组缺失突变体在HBV各编码区及基因调控区均存在不同程度缺失,其中66%(42/64种)保留与HBV复制(包装)相关的所有顺式调控序列,48%(31/64种)保留X编码区.结论 乙型肝炎患者血清中普遍存在小分子HBV基因组缺失突变体,深入了解这些变异体的结构和功能,有助于进一步探索HBV的致病机制.
目的 瞭解小分子HBV基因組缺失突變體的基因結構及特點.方法 採用一步法PCR從慢性乙型肝炎患者血清中擴增全基因組HBV DNA,迴收併剋隆＜1 kh的小分子HBV DNA,測序併以BioEdit及VectorNTI 6.0軟件分析基因結構特點.結果 穫得基因長度介于174～986 bp之間的64種、共124箇小分子HBV缺失突變體DNA,按基因結構特點分為3類,即3種GT-AG剪接變異體、29種"常規"缺失突變體及32種基因組內部含polyA的缺失突變體.所有小分子基因組缺失突變體在HBV各編碼區及基因調控區均存在不同程度缺失,其中66%(42/64種)保留與HBV複製(包裝)相關的所有順式調控序列,48%(31/64種)保留X編碼區.結論 乙型肝炎患者血清中普遍存在小分子HBV基因組缺失突變體,深入瞭解這些變異體的結構和功能,有助于進一步探索HBV的緻病機製.
목적 료해소분자HBV기인조결실돌변체적기인결구급특점.방법 채용일보법PCR종만성을형간염환자혈청중확증전기인조HBV DNA,회수병극륭＜1 kh적소분자HBV DNA,측서병이BioEdit급VectorNTI 6.0연건분석기인결구특점.결과 획득기인장도개우174～986 bp지간적64충、공124개소분자HBV결실돌변체DNA,안기인결구특점분위3류,즉3충GT-AG전접변이체、29충"상규"결실돌변체급32충기인조내부함polyA적결실돌변체.소유소분자기인조결실돌변체재HBV각편마구급기인조공구균존재불동정도결실,기중66%(42/64충)보류여HBV복제(포장)상관적소유순식조공서렬,48%(31/64충)보류X편마구.결론 을형간염환자혈청중보편존재소분자HBV기인조결실돌변체,심입료해저사변이체적결구화공능,유조우진일보탐색HBV적치병궤제.
Objective To elucidate the genome organization of small deletion mutants of hepatitis B virus(HBV).Methods Amplified the HBV genomes by polymerase chain reaction from the serum of the patients with chronic hepatitis B and cloned the small HBV DNA less than 1 kb,then sequenced and analyzed the gene organization of these small deletion mutants of HBV.Results Totally one hundred and twenty-four small deletion mutants of HBV genomes categorized to sixty-four types were obtained and classified into three groups according to the criteria of the characteristics of gene organization,for example,spliced variants,regular deletion mutants and the deletion mutants with an internal poly (dA).All of these isolated mutants shared some common features as the deletion in coding regions and regulatory elements,66% of the mutants retained the cis elements crucial for the viral replication and encapsidation,while 48% retained the X region.Conclusions Small deletion mutants of HBV are commonly detected in the serum from chronic hepatitis B patients,the characteristic structure of such mutants implies that they might be closely co-related with the pathogenicity of HBV.The exact mechanisms need further study yet.
