南京大学学报(自然科学版)
南京大學學報(自然科學版)
남경대학학보(자연과학판)
JOURNAL OF NANJING UNIVERSITY(NATURAL SCIENCES)
2005年
5期
451-461
,共11页
刘建宁%张德正%Carole LeContel%陈平%Victor Gurewich%张菁%陈新园
劉建寧%張德正%Carole LeContel%陳平%Victor Gurewich%張菁%陳新園
류건저%장덕정%Carole LeContel%진평%Victor Gurewich%장정%진신완
尿激酶%HIV-1%gp120%V3环区%纤溶酶原%人体免疫缺损病毒
尿激酶%HIV-1%gp120%V3環區%纖溶酶原%人體免疫缺損病毒
뇨격매%HIV-1%gp120%V3배구%섬용매원%인체면역결손병독
HIV-1%urokinase%gp120%plasminogen%v3 loop%AIDS
人体免疫缺损病毒的包膜蛋白gp120的V3环区包含一段在人类蛋白质中很少出现的高度保守序列,但这段序列与纤溶酶原被纤溶酶原激活剂酶切位点附近序列有同源性.由于V3环区在人体免疫缺损病毒侵染细胞过程中的重要性,评估了尿激酶对人体免疫缺损病毒侵染能力的影响.通过检测逆转录酶活力,P24抗原的表达和合胞体形成情况发现尿激酶可以抑制人体免疫缺损病毒对多种淋巴瘤和白血病细胞系,如MT4、CEM、H9和外周血单核细胞的侵染能力,并且这种抑制与尿激酶浓度呈剂量依赖关系.那些能够被尿激酶抑制的人体免疫缺损病毒株其V3环区序列必须与纤溶酶原激活区序列同源,实验室常用病毒株包括BRU和RF以及某些野生病毒株.研究结果显示尿激酶在体外实验中可以抑制人体免疫缺损病毒的侵染能力.
人體免疫缺損病毒的包膜蛋白gp120的V3環區包含一段在人類蛋白質中很少齣現的高度保守序列,但這段序列與纖溶酶原被纖溶酶原激活劑酶切位點附近序列有同源性.由于V3環區在人體免疫缺損病毒侵染細胞過程中的重要性,評估瞭尿激酶對人體免疫缺損病毒侵染能力的影響.通過檢測逆轉錄酶活力,P24抗原的錶達和閤胞體形成情況髮現尿激酶可以抑製人體免疫缺損病毒對多種淋巴瘤和白血病細胞繫,如MT4、CEM、H9和外週血單覈細胞的侵染能力,併且這種抑製與尿激酶濃度呈劑量依賴關繫.那些能夠被尿激酶抑製的人體免疫缺損病毒株其V3環區序列必鬚與纖溶酶原激活區序列同源,實驗室常用病毒株包括BRU和RF以及某些野生病毒株.研究結果顯示尿激酶在體外實驗中可以抑製人體免疫缺損病毒的侵染能力.
인체면역결손병독적포막단백gp120적V3배구포함일단재인류단백질중흔소출현적고도보수서렬,단저단서렬여섬용매원피섬용매원격활제매절위점부근서렬유동원성.유우V3배구재인체면역결손병독침염세포과정중적중요성,평고료뇨격매대인체면역결손병독침염능력적영향.통과검측역전록매활력,P24항원적표체화합포체형성정황발현뇨격매가이억제인체면역결손병독대다충림파류화백혈병세포계,여MT4、CEM、H9화외주혈단핵세포적침염능력,병차저충억제여뇨격매농도정제량의뢰관계.나사능구피뇨격매억제적인체면역결손병독주기V3배구서렬필수여섬용매원격활구서렬동원,실험실상용병독주포괄BRU화RF이급모사야생병독주.연구결과현시뇨격매재체외실험중가이억제인체면역결손병독적침염능력.
The V3 loop of the envelope protein, gp120, of HIV-1 contains a highly conserved motif, which is rare in human proteins, but we noted that it was homologous to the activation site loop of plasminogen that is cleaved by plasminogen activators. Since the V3 loop is important to cell entry of HIV-1, the effect of urokinase on HIV-1 infectivity was evaluated. When HIV-1 in culture medium was exposed to a range of concentrations of urokinase, a dose-dependent inhibition of infectivity was observed in a variety of lymphoma and leukemia cell lines including MT4, CEM, H9, and peripheral blood mononuclear cells using assays for reverse transcriptase, P24 antigen and syncytia formation. The HIV-1 strains inhibited by UK were those whose V3 loops were homologous to plasminogen and included the laboratory strains BRU and RF, as well as certain wild strains. In conclusion, the present study shows that UK inhibits infectivity by HIV-1 in vitro.