HCV的检测方法

从发现丙型肝炎病毒以来 ,丙肝的检测技术发展迅速 ,灵敏度和特异性都有明显的提高 ,方法学在不断改进完善。笔者就近年来丙型肝炎的实验室检测方法作简要的综述     

HBV-M定量检测与HBV-DNA含量水平关系的初步探讨

目的 研究乙型肝炎病毒标志物定量检测结果与其HBV-DNA含量的临床关系。方法 采用时间分辨免疫定量和荧光定量-PCR技术，对HBV-DNA和HBV-DNA含量进行检测。结果 在HBsAg/HBeAg/HBcAb,HBsAg/HBcAb/HBcAb,HBeAg/IC及单纯HBcAb阳性的四个组别中，HBV-DNA阳性率分别是97.17%、30.56%、100%和25%；在HBsAg,HBeAg,HBeAb,HBcAb定量检测高，低值两组HBV-DNA含量对比中，HBV-DNA阳性率分别为76.92%、58.14%；100%、97.26%；20.00%、11.42%；64.62%、27.63%。结论 HBV-DNV比HBV-M更能及时准确反映乙型肝炎病毒感染者的病程情况。     

LightCycler实时监测PCR定量分析血清HBV DNA

目的 检验LightCycler实时监测PCR（real-time detection PCR,RTD-PCR)对血清中HBV DNA定量检测的灵敏性和可重复性，探讨HBV血清标志物与HBV DNA定量的关系。方法 HBV定量按深圳匹基公司乙肝PCR荧光检测试剂盒使用说明，对乙肝标志物已明确的773例血清中HBV DNA定量结果进行统计分析。结果 实时监测PCR对血清中HBV DNA定量检测的灵敏性高，可检测低至1000拷贝／ml血清；可重复性好，批间误差＜20％；各种标志物类型的血清HBV DNA含量分布情况表明，HBV血清标志物中HBeAg与HBV DNA含量有明显的关系，一般HBeAg阳性血清HBV DNA含量较高，但也有相当一部分例外。结论 LightCycler实时监测PCR对血清中HBV DNA定量检测灵敏性高可重复性好；仅根据HBV血清标志物往往不能确定乙肝患者HBV DNA复制水平的高低，HBV DNA定量检测具有十分重要的临床意义。     

Spinal MRI in vacuolar myelopathy, and correlation with histopathological findings

We correlated MRI features with histopathological findings in an HIV-positive patient with vacuolar myelopathy. On MRI symmetrical nonenhancing high-signal areas in the posterior columns on T2-weighted images result from extensive vacuolation visible on histological sections. Received: 18 November 1997 Accepted: 23 March 1997     

新生儿先天性畸形与孕妇乙型肝炎病毒感染关系的研究

为探讨孕妇乙型肝炎病毒(HBV)感染和某些因素对先天性畸形的致病作用,本文进行了96对新生儿先天畸形的配对(1:1)病例对照研究,报道先天畸形的频率和构成,单因素和多因素的条件Logistic回归分析,表明孕妇HBsAg阳性等6个因素对先天畸形呈阴性结果,而与接触农药和孕周的因素有明显联系,值得进一步探讨。     

HIV neuropathogenesis and therapeutic strategies

Abstract Human immunodeficiency virus (HIV)-l neuropathogenesis can be divided into three important components: (i) virus entry into the nervous system; (ii) the role of viral proteins and/or cellular products in neural tissue damage; and (iii) the mechanisms of neuronal injury/death. Both blood derived macrophages or trafficking HIV-1 infected T-lymphocytes have been implicated in viral entry to the central nervous system (CNS). The major cell type harboring productive HIV-1 infection in the nervous system is the perivascular macrophage/ microglia. The HIV-1 infection of brain astrocytes, restricted to the expression of regulatory gene products, may cause astrocyte dysfunction and contribute to neuronal injury or to disruption of the blood-brain barrier (BBB). Studies of cerebrospinal fluid and postmortem tissues reveal chronic inflammation/immune activation in the nervous system during the later stages of HIV-1 infection associated with disruption of BBB integrity. Blood-brain barrier damage may underlie the white matter pallor described in HIV-1 infection and could result in further entry into the CNS of toxic viral or cellular products, or additional HIV-1 infected cells. The HIV infected and activated macrophages/microglia produce excessive amounts of pro-inflammatory cytokines, including tumor necrosis factor alpha, and platelet activating factor. These products are directly toxic to human neurons in vitro. The HIV-1 envelope glycoprotein, gp 120 may stimulate the release of toxic factors from brain macrophages. Blocking N-methyl-D-aspartate (NMDA; or AMPA) glutamate receptors can antagonize candidate toxins of both viral and cellular origin. It has been postulated that (weak) excitotoxicity leads to oxidative stress in neurons and ultimately to apoptosis. Neuronal apoptosis occurs in the brains of both children and adults with HIV-1 infection. This understanding of HIV neuropathogenesis implies that therapeutic strategies should include: (i) anti-retroviral medications to decrease systemic and CNS virus load, and possibly to prevent perinatal transmission of HIV; (ii) anti-inflammatory compounds to decrease the chronic immune activation in microglia and allow the restoration of BBB integrity; and (iii) neuroprotective compounds to reduce neuronal injury and apoptotic death.     

Detection of hepatocellular carcinoma after interferon therapy for chronic hepatitis C: Clinical study of 26 cases

The clinical findings in 26 patients in whom hepatocellular carcinoma (HCC) was detected after the start of interferon (IFN) therapy for chronic hepatitis C were analysed. Histological study before IFN therapy showed that 34.6% of patients were categorized as stage 3 (septal fibrosis with architectural distortion; the 0–4 scale) and 80.8% demonstrated at least some evidence of septal fibrosis or more advanced features. The AFP levels examined before IFN therapy were more than 20 ng/mL in 13 patients (84.6% of those studied). One of 26 patients had a complete response to IFN therapy, while six of 26 patients had only a partial response. HCC was detected within 1 year after the start of IFN therapy in 76.9% of patients. Thus, the possibility of the early occurrence of HCC or its existence at the time of therapy should be seriously considered when IFN therapy is contemplated. Patients with stage 3 or 3–4 histology may already have a small undetectable HCC before IFN therapy. Thus, for this reason, every patient treated with IFN should be examined at short regular intervals for the development of HCC during and after IFN therapy.     

110例嗜酸细胞增多性非变应性鼻炎的液氮冷冻治疗

１１０例嗜酸细胞增多性非变应性鼻炎的液氮冷冻治疗山西医学院第二附属医院（０３０００１）牛玉梅，刘学仁按Ｍｇｇｉｎｄ将常年性鼻炎分为三类：一类常年性变态反应性鼻炎；二类非变态反应性鼻炎伴鼻分泌物嗜酸细胞增多综合征也叫嗜酸细胞增多性非变态反应性鼻炎（Ｅｏｓｉｎｏｐｈｉｌｉｃｎｏｎａｌｌｅｒａｉｃｒｈｉｎｉｔｓ，ＥＮＲ）；三类自主神经性常年性鼻炎［１］。我们将ＥＮＲ中找不到致敏物，而与冷热空气有关与情绪无关的１１０例患者进行了液氮冷冻治疗。临床资料８０２例常年性鼻炎患者进行皮肤激发试验。４３７例找出了致敏物，进行特异性过敏诱因脱敏治疗或抗过敏药物治疗。３６５例试验阳性，其中有１３５例与冷热空气有关。ｌｌ０例行冷冻治疗。１ｌ０例中男５０例，女６０例；年龄最大６５岁，最小１６岁。１１０例均有间歇性的连续喷嚏发作，浆液性或粘液性鼻分泌物增多和鼻粘膜非充血性肿胀引起的堵塞，无因吸入致敏原诱发症状的病史；血清ＩｇＥ值不升高，特异性皮肤试验结果为阳性；鼻分泌物中嗜酸细胞阳性。方法：先将鼻腔内喷入１％地卡因溶液３次粘膜表面麻醉，用卷好的４厘米长、０．４～０．６厘米粗的棉棒沾上液氮在鼻镜直视下迅速插入鼻腔内。时间约１分钟左右（冷     

HCV HVR1准种在不同基因型丙型肝炎患者中的分布

目的:通过研究丙型肝炎病毒高变区1(HCV HVR1)准种复杂性与基因型之间的关系,探讨不同基因型HCV致病性差异的机制.方法:采用C区型特异性引物PCR法进行HCV基因分型,采用单链构象多态性聚合酶链反应法(SSCP法)检测HCV HVR1准种.结果:68例丙型肝炎患者中,Ⅱ型49例(72%),Ⅲ型13例(19%),Ⅱ、Ⅲ混合型6例(9%).Ⅱ型和Ⅱ、Ⅲ混合型HCV感染患者的HCV HVR1准种复杂性(SSCP条带数)明显高于Ⅲ型感染的患者,且与疾病严重程度关系密切.结论:HCV HVR1准种复杂性的差异可能是导致不同基因型HCV致病性差异的因素之一.     

抗戊型肝炎病毒重组蛋白单克隆抗体的制备和初步应用

目的:制备抗-戊型肝炎病毒的单克隆抗体,并将其用于分析戊型肝炎病毒不同毒株结构蛋白的抗原表位。方法:采用来自墨西哥株(Mexicanstrain)的戊型肝炎病毒重组蛋白(p166Mex)免疫Balb/c小鼠,取其脾细胞与SP2/0骨髓瘤细胞进行融合,经酶联免疫吸附试验(ELISA)法筛选阳性克隆,并将获得的单克隆抗体与戊型肝炎病毒缅甸株(Burmastrain)和美国株(USAstrain)的重组蛋白(p166Bur、p166US)进行交叉反应测定。结果:最终获得4株能稳定分泌抗-p166Mex的杂交瘤细胞株,即D8G10、E5E12、D4A3、B7E6。其中D8G10,E5E12和B7E6细胞株的培养上清液,还能分别与p166Bur和p166US重组蛋白发生阳性反应。结论:利用已获得的抗-p166Mex单克隆抗体,初步确定3种不同的戊型肝炎病毒重组蛋白(p166Bur、p166US、p166Mex)含有一种共同的抗原表位。