中南大学学报(医学版)
中南大學學報(醫學版)
중남대학학보(의학판)
JOURNAL OF CENTRAL SOUTH UNIVERSITY (MEDICAL SCIENCES)
2011年
11期
1052-1058
,共7页
陈莉%李聪智%孟秀娟%朱平安%谭德明
陳莉%李聰智%孟秀娟%硃平安%譚德明
진리%리총지%맹수연%주평안%담덕명
DC-SIGN%乙型肝炎病毒%乙型肝炎,慢性%启动区%突变
DC-SIGN%乙型肝炎病毒%乙型肝炎,慢性%啟動區%突變
DC-SIGN%을형간염병독%을형간염,만성%계동구%돌변
DC-SIGN%hepatitis B virus%hepatitis B,chronic%promoter region%mutation
目的:了解慢性乙型肝炎(chronic hepatitis B,CHB)患者与既往乙型肝炎病毒(hepatitis B virus,HBV)感染者体内树突状细胞特异性细胞间黏附分子-3结合非整合素因子(dendritic cell-specific intercellular adhension molecule-3-grabbing nonintegrin,DC-SIGN)启动区基因变异情况,探讨DC-SIGN启动区基因变异与HBV的关系.方法:采用PCR,单链构象多态性与异源性分析,及分子克隆、测序、比对等方法对47例CHB患者与20例既往HBV感染者体内DC-SIGN启动区基因变异进行分析.结果:HBV感染者体内特异性的DC-SIGN启动区存在基因变异.在CHB患者,DC-SIGN启动区有4个位点出现突变(- 139,- 142,- 222,- 336).然而在既往HBV感染者,仅- 139位点出现突变.11例CHB患者表现为- 336C(23.40%),但是在既往HBV感染者未观察到该表现型.所有的既往HBV感染者均表现为- 139T( 100%),而仅34.04%的CHB患者表现为- 139T.结论:DC-SIGN启动区内- 336C表现型可能是CHB的危险因素之一,而- 139T表现型可能具有增强机体对抗HBV的作用.
目的:瞭解慢性乙型肝炎(chronic hepatitis B,CHB)患者與既往乙型肝炎病毒(hepatitis B virus,HBV)感染者體內樹突狀細胞特異性細胞間黏附分子-3結閤非整閤素因子(dendritic cell-specific intercellular adhension molecule-3-grabbing nonintegrin,DC-SIGN)啟動區基因變異情況,探討DC-SIGN啟動區基因變異與HBV的關繫.方法:採用PCR,單鏈構象多態性與異源性分析,及分子剋隆、測序、比對等方法對47例CHB患者與20例既往HBV感染者體內DC-SIGN啟動區基因變異進行分析.結果:HBV感染者體內特異性的DC-SIGN啟動區存在基因變異.在CHB患者,DC-SIGN啟動區有4箇位點齣現突變(- 139,- 142,- 222,- 336).然而在既往HBV感染者,僅- 139位點齣現突變.11例CHB患者錶現為- 336C(23.40%),但是在既往HBV感染者未觀察到該錶現型.所有的既往HBV感染者均錶現為- 139T( 100%),而僅34.04%的CHB患者錶現為- 139T.結論:DC-SIGN啟動區內- 336C錶現型可能是CHB的危險因素之一,而- 139T錶現型可能具有增彊機體對抗HBV的作用.
목적:료해만성을형간염(chronic hepatitis B,CHB)환자여기왕을형간염병독(hepatitis B virus,HBV)감염자체내수돌상세포특이성세포간점부분자-3결합비정합소인자(dendritic cell-specific intercellular adhension molecule-3-grabbing nonintegrin,DC-SIGN)계동구기인변이정황,탐토DC-SIGN계동구기인변이여HBV적관계.방법:채용PCR,단련구상다태성여이원성분석,급분자극륭、측서、비대등방법대47례CHB환자여20례기왕HBV감염자체내DC-SIGN계동구기인변이진행분석.결과:HBV감염자체내특이성적DC-SIGN계동구존재기인변이.재CHB환자,DC-SIGN계동구유4개위점출현돌변(- 139,- 142,- 222,- 336).연이재기왕HBV감염자,부- 139위점출현돌변.11례CHB환자표현위- 336C(23.40%),단시재기왕HBV감염자미관찰도해표현형.소유적기왕HBV감염자균표현위- 139T( 100%),이부34.04%적CHB환자표현위- 139T.결론:DC-SIGN계동구내- 336C표현형가능시CHB적위험인소지일,이- 139T표현형가능구유증강궤체대항HBV적작용.
To investigate whether there is mutation in DC-SIGN promoter region in patients with chronic hepatitis B (CHB) and healthy persons previously infected with hepatitis B virus (HBV) and to explore the relationship between the mutation in dendritic cell-specific intercellular adhension molecule-3-grabbing nonintegrin (DC-SIGN) promoter region and HBV.Methods The studied population was composed of two cohorts:47 CHB patients and 20 healthy persons previously infected with HBV.The mutation in DC-SIGN promoter region was detected with PCR,single-stranded conformational polymorphism and heteroduplex analysis,cloning,sequencing and aligning the published DC-SIGN promoter sequence.Results The characteristic mutation within DCSIGN promoter region in HBV infected individuals was observed.In the DC-SIGN promoter region,4 hot spot mutations located in positions - 139,- 142,- 222,and - 336 were observed in the CHB patients,but only 1 spot mutation located in position - 139 was observed in the healthy persons previously infected with HBV.The -336C which was absent in the healthy persons previously infected with HBV was shown in 11 CHB patients (23.40%).The - 139T was far more frequent in the healthy persons previously infected with HBV ( 100% ) than in the CHB patients (34.04%).Conclusion In the DC-SIGN promoter region,-336C may be a genetic risk factor for developing CHB,but -139T may be associated with protection against HBV.