慢性肾盂肾炎发病与巨细胞病毒感染关系初探

应用免疫酶斑点法检测慢性肾盂肾炎病人尿液中巨细胞颊毒，同时应用ＥＬＩＳＡ法检测血中ＨＣＭＶ抗体，检测结果表明，尿中ＨＣＭＶ阳性率为５２．９％，血清中ＨＣＭＶ抗体为７５．９％，与正常对照组相比，并差非常显著，证明慢性肾盂炎发病与ＨＣＭＶ感染有关。     

巢式PCR检测龈下菌斑中HCMV、EBV、HSV-1与慢性牙周炎活动性的关系

目的　建立临床检测龈下菌斑标本中人巨细胞病毒 (HCMV)、Epstein Barr病毒 (EBV)、单纯疱疹病毒 1型 (HSV 1 )巢式PCR方法 ,研究这 3种病毒与慢性牙周炎活动性的关系。方法　收集6 2例慢性牙周炎患者 (男性 2 7例、女性 35例 ,平均年龄 5 3岁 )的牙周炎活动部位、牙周炎静止部位的龈下菌斑 ,提取DNA后使用巢式PCR检测HCMV、EBV、HSV 1 ,比较分析其在同一病人不同部位的检出率。结果　牙周炎活动部位的HCMV检出率为 38.7%,EBV的检出率为 5 8%,HSV 1的检出率为30 .6 %,两种以上病毒合并感染的检出率为 4 0 .3%;牙周炎静止部位的HCMV检出率为 1 4 .5 %,EBV为 2 2 .6 %,HSV 1为 1 1 .3%,两种以上病毒合并感染的检出率为 1 1 .3%。这 3种病毒及其合并感染在牙周炎活动部位的检出率均高于牙周炎静止部位 ,差异有统计学意义 (P <0 .0 5 )。结论　提示HC MV、EBV、HSV 1与慢性牙周炎的活动性相关。     

白血病患者巨细胞病毒抗体检测及其临床意义初探

目的初步探讨白血病患者巨细胞病毒(HCMV)感染状况及HCMV抗体检测的应用价值.方法采用ELISA法对75例白血病患者和28名健康人HCMV抗体进行检测.其中有11例M3患者作化疗前后对比检测.结果白血病组HCMV-IgM抗体阳性率为2.7%,健康对照组为0;白血病组HCMV-IgG抗体水平较健康对照组显著(P＜0.01)或非常显著(P＜0.005)增高;如以HCMV-IgG抗体高于8.4IU/ml(约临界值1.1IU/ml的4倍)考虑为HCMV活动性感染,则白血病组阳性率35.7%,较健康对照组3.6%明显升高(P＜0.005),且M3化疗后阳性率有上升趋势.结论HCMV抗体检测有助于白血病患者HCMV感染的临床诊疗.     

生命泉流浸膏体外抗HSV-2和HCMV作用的实验研究

以无环鸟苷 ( ACV)和病毒唑 ( RBV)作阳性对照物 ,采用 MTT法和细胞病变 ( CPE)抑制法 ,观察了生命泉流浸膏( FESOL)抗单纯疱疹病毒 型 ( HSV-2 )和人巨细胞病毒 ( HCMV)的作用效果     

套式聚合酶链反应及限制酶分析检测新生儿肝炎巨细胞病毒感染

在人巨细胞病毒（HCMV）AD169株直接早期蛋白EcoRIJDNA片段内，自行设计二对引物，建立套式PCR检测HCMVDNA。经实验证明有高度的特异性与敏感性，对其它疙疹类病毒和正常人基因组DNA无交叉反应。一次性PCR检测HCMVAD169株基因组的最小检出量为100fg，而套式PCR可达10fg，经PStI酶切后，得到的片段与设计相符。对23例新生儿肝炎临床标本进行病毒分离，一次性PCR，套式PCR检测，结果表明套式PCR能进一步提高一次性PCR的特异性与敏感性，适用于新生儿肝炎HCMV感染的临测。     

HCMV感染介导的椎间盘组织退变模型的病理学观察

目的 探讨HCMV感染Balb/c小鼠对椎间盘退变及病理学改变的模型研究,活体Balb/c小鼠模型导入组织学、基因表达、免疫学的研究,确定人巨细胞病毒注射到腹腔对椎间盘退变的影响及不同剂量的对照性研究。方法 （1）随机选取6-8周SPF级Balb/c小鼠84只,建立五个不同感染量HCMVAD169株感染Balb/c小鼠模型雌雄各6只为感染组（A组）,同时设立病毒灭活组（B组）和细胞对照组（C组）雌雄各6只;（2）间接ELISA法检测小鼠血清中的IgG、IgM抗体水平,取各组小鼠椎间盘组织进行病毒分离,采用PCR和RT-PCR分别检测HCMVUL83基因和UL54基因转录产物;（3）取各组小鼠椎间盘组织行病理学观察。结果 A组和B组小鼠IgG抗体均为阳性,C组为阴性,小鼠IgM抗体仅A组中2×106PFU/ml和2×105PFU/ml感染组雌性小鼠为阳性;上述两感染组小鼠病毒分离、PCR及RT-PCR均为阳性,病理学可见椎间盘组织髓核细胞数目减少,排列不均匀,纤维环结构紊乱;雄性小鼠、其余A组、B组和C组均无明显变化。结论 HCMV注射后似乎能逐渐诱导椎间盘退变,出现病理学改变;该模型对椎间盘退变的分子水平研究有显著的优势;进一步研究将会阐述HCMV介导椎间盘退变相关的分子学等机制和过程。     

婴幼儿巨细胞病毒临床分离株的流行病学研究

目的:分析湖南省婴幼儿巨细胞病毒临床分离株的疾病类型构成及发病特点。方法:用人胚肺成纤维细胞(HEL)培养0-1岁患儿HCMVDNA阳性的尿液,共分离到29例病毒阳性者,对照患儿入院时的肝功能、血常规等指标及出院时的诊断,展开病原性调研。调查表明在婴幼儿神经脑损伤、肺炎、肝炎、结肠炎、肠炎、低蛋白血症、败血症等患者中都分离到了人类巨细胞病毒;扩增了29例分离到的HCMV的gB基因,并对其基因型进行了分析。结论:婴幼儿HCMV临床分离株的疾病类型分布广泛,HCMV是婴幼儿神经脑损伤等多种疾病的诱发因素,湖南省婴幼儿HCMV的感染以gBⅠ型为优势基因型。     

HCMV Infection of Human Trophoblast Progenitor Cells of the Placenta Is Neutralized by a Human Monoclonal Antibody to Glycoprotein B and Not by Antibodies to the Pentamer Complex

Human cytomegalovirus (HCMV) is the major viral cause of congenital infection and birth defects. Primary maternal infection often results in virus transmission, and symptomatic babies can have permanent neurological deficiencies and deafness. Congenital infection can also lead to intrauterine growth restriction, a defect in placental transport. HCMV replicates in primary cytotrophoblasts (CTBs), the specialized cells of the placenta, and inhibits differentiation/invasion. Human trophoblast progenitor cells (TBPCs) give rise to the mature cell types of the chorionic villi, CTBs and multi-nucleated syncytiotrophoblasts (STBs). Here we report that TBPCs are fully permissive for pathogenic and attenuated HCMV strains. Studies with a mutant virus lacking a functional pentamer complex (gH/gL/pUL128-131A) showed that virion entry into TBPCs is independent of the pentamer. In addition, infection is blocked by a potent human neutralizing monoclonal antibody (mAb), TRL345, reactive with glycoprotein B (gB), but not mAbs to the pentamer proteins pUL130/pUL131A. Functional studies revealed that neutralization of infection preserved the capacity of TBPCs to differentiate and assemble into trophospheres composed of CTBs and STBs in vitro. Our results indicate that mAbs to gB protect trophoblast progenitors of the placenta and could be included in antibody treatments developed to suppress congenital infection and prevent disease.     

Herpesvirus-encoded GPCRs rewire cellular signaling

Viral G-protein-coupled receptors (vGPCRs) are chemokine receptor homologues encoded by the Herpes- and Capripoxviridae. They are thought to have been hijacked from the host genome during the course of evolution. These vGPCRs play different roles in the viral lifecycle and associated pathologies. Three members of the Herpesviridae, Kaposi sarcoma-associated herpesvirus (KSHV), Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) are capable of setting up persistent latent infections in humans. Two of the herpesviruses, KSHV and EBV, are associated with cancer, while HCMV may have an oncomodulary effect.     

Proteasome-dependent, ubiquitin-independent degradation of Daxx by the viral pp71 protein in human cytomegalovirus-infected cells

The cellular Daxx protein represses human cytomegalovirus (HCMV) gene expression from the major immediate early promoter. HCMV prevents Daxx-mediated silencing during lytic infection by delivering the viral pp71 tegument protein to the nucleus, where pp71 binds to and induces the proteasomal degradation of Daxx. In this study, we show that a functional ubiquitin pathway is not required for the proteasomal degradation of the endogenous Daxx protein by tegument-delivered pp71 in HCMV-infected cells, demonstrating that the pp71-mediated degradation of Daxx occurs through a proteasome-dependent, ubiquitin-independent pathway.