CAJ | 학술논문

目的检测SLE患者外周血人巨细胞病毒(HCMV)的感染状况,探讨HCMV感染在SLE发病中的作用.方法采集并抽提60例已确诊的SLE患者和1 1 1名健康人外周血白细胞DNA,利用巢式PCR技术检测HCMV糖蛋白gB(UL55)基因以确定HCMV感染情况.应用2个独立样本t检验、非参数检验、x2检验及Fisher确切概率法统计分析.结果琼脂糖凝胶电泳及测序显示建立的巢式PCR能特异地检测HCMV-UL55基因,SLE患者外周血中HCMV检出率明显高于对照组[分别为41.7％(25/60)和1.8％(2/111),x2=46.551,P＜0.01].与外周血HCMV阴性组SLE患者相比,HCMV阳性组SLE患者抗核糖体P蛋白抗体(Rib-P)阳性率[分别为26％ (9/35),56％(14/25),x2=5.659,P=0.017]、直接Coomb's试验阳性率[分别为37％(13/35),72％(18/25),x2=7.096,P=0.008]及抗β2糖蛋白1(GP1)抗体水平[分别为21.3(9.9,51.8) U/ml,13.6(5.9,23.1) U/ml;U=2.017,P=0.044]明显升高,血液系统相关指标中的红细胞[分别为(3.65±0.10)×1012/L,(3.17±0.17)×1012/L; t=2.574,P=0.013]、淋巴细胞[分别为(1.37±0.14)×1012/L,(0.90±0.13)×1012/L;t=2.456,P=0.017]、血红蛋白[分别为(110±19) g/L,(98±5) g/L;t=2.034,P=0.048]明显减少;肾损害相关指标中的血尿阳性率[分别为40％(14/35),72％(18/25);x2=6.000,P=0.014]、尿蛋白定量(24h)水平[分别为0.80(0.53,2.37)g,0.48(0.13,1.21)g;U=2.140,P=0.032]明显上升.结论外周血细胞HCMV感染可能参与SLE发生、发展过程.
목적 검측SLE환자외주혈인거세포병독(HCMV)적감염상황,탐토HCMV감염재SLE발병중적작용.방법 채집병추제60례이학진적SLE환자화1 1 1명건강인외주혈백세포DNA,이용소식PCR기술검측HCMV당단백gB(UL55)기인이학정HCMV감염정황.응용2개독립양본t검험、비삼수검험、x2검험급Fisher학절개솔법통계분석.결과 경지당응효전영급측서현시건립적소식PCR능특이지검측HCMV-UL55기인,SLE환자외주혈중HCMV검출솔명현고우대조조[분별위41.7％(25/60)화1.8％(2/111),x2=46.551,P＜0.01].여외주혈HCMV음성조SLE환자상비,HCMV양성조SLE환자항핵당체P단백항체(Rib-P)양성솔[분별위26％ (9/35),56％(14/25),x2=5.659,P=0.017]、직접Coomb's시험양성솔[분별위37％(13/35),72％(18/25),x2=7.096,P=0.008]급항β2당단백1(GP1)항체수평[분별위21.3(9.9,51.8) U/ml,13.6(5.9,23.1) U/ml;U=2.017,P=0.044]명현승고,혈액계통상관지표중적홍세포[분별위(3.65±0.10)×1012/L,(3.17±0.17)×1012/L; t=2.574,P=0.013]、림파세포[분별위(1.37±0.14)×1012/L,(0.90±0.13)×1012/L;t=2.456,P=0.017]、혈홍단백[분별위(110±19) g/L,(98±5) g/L;t=2.034,P=0.048]명현감소;신손해상관지표중적혈뇨양성솔[분별위40％(14/35),72％(18/25);x2=6.000,P=0.014]、뇨단백정량(24h)수평[분별위0.80(0.53,2.37)g,0.48(0.13,1.21)g;U=2.140,P=0.032]명현상승.결론 외주혈세포HCMV감염가능삼여SLE발생、발전과정.
Objective To detect the prevalence of human cytomegalovirus (HCMV) in peripheral blood of patients with systemic lupus erthematosus (SLE) and explore its role in the pathogenesis of SLE.Methods HCMV DNA was isolated from the peripheral blood leucocytes (PBLs) of 60 patients with SLE and 111 healthy controls.Nested polymerase chain reaction (nPCR) technology was used to investigate the gene of HCMV glycoprotein gB (UL55) in these specimens.HCMV infections in the PBLs of SLE patients were confirmed by HCMV-UL55 detection.Two-sample t test,nonparametric test,Chi-square test and Fisher probabilities were used to analyze.Results Agarose gel electrophoresis and sequencing analysis showed that established nPCR could specifically detect HCMV-UL55 gene,the HCMV infection rate was significantly higher in patients with SLE than in the healthy controls (P＜0.01).Positive rates of HCMV infection in SLE group and controls were 41.7％ (25/60) and 1.8％ (2/111),respectively.Compared to the SLE patients with HCMV-negative PBLs,the positive rate of Rib-P [26％(9/35) vs 56％(14/25),x2=5.659,P=0.017],the positive rate of direct Coomb's test [37％(13/35) vs 72％(18/25),x2=7.096,P=0.008] and the level of antiβ2GP1 [21.3 (9.9,51.8) U/ml vs 13.6 (5.9,23.1) U/ml,U=2.017,P=0.044] were significantly higher than those in the SLE patients with HCMV-positive PBLs.Compared to the SLE patients with HCMV-negative PBLs,the number of red blood cells [(3.65±0.10)×1012/L vs (3.17±0.17)×1012/L,t=2.574,P=0.013] and lymphocytes [(1.37±0.14)×1012/L vs (0.90±0.13)×1012/L,t=2.456,P=0.017] in peripheral blood and the hemoglobin levels [(110±19) g/L vs (98±5)g/L,t=2.034,P=0.048] of the SLE patients with HCMV-positive decreased significantly.At the same time,the positive rate of hematuria [40％(14/35) vs 72％(18/25),x2=6.000,P=0.014] and 24 h proteinuria [0.80 (0.53,2.37)g vs 0.48 (0.13,1.21)g,U=2.140,P=0.032],which indicated kidney damage were also significantly increased in SLE patients with HCMV-positive PBLs.Conclusion The infection of HCMV in peripheral blood cells may take part in the development of SLE.