Hepatitis C and steatosis

Hepatitis C infection and non-alcohol-related hepatic steatosis are the most common liver diseases worldwide, and both conditions often co-exist in the same patient. Hepatitis C virus (HCV) genotype 3 directly induces development of steatosis, whereas in patients with non-genotype 3 chronic hepatitis C infection, insulin resistance plays a key role in the pathophysiology of steatosis. Insulin resistance and its clinical components including obesity, hyperglycemia, hypertriglyceridemia, increased blood pressure, and low HDL-cholesterol levels are often seen in patients with chronic hepatitis C infection. Both increased adipocity and presence of steatosis may increase the risk of fibrosis progression, and both have been associated with a decreased rate of response to antiviral treatment. Hence, liver steatosis in the setting of HCV infection is a distinct condition with specific clinical and prognostic implications. Accumulating evidence suggests that weight management may lead not only to a decrease in steatosis but also improvement in fibrosis severity. However, further studies are necessary to determine whether weight reduction improves response to antiviral therapy.     

Hepatitis C in childhood

The prevalence of hepatitis C virus (HCV) infection is relatively low in childhood. Blood transfusion has been the principal route of acquisition in children but vertical transmission is gradually occupying primacy in the developed world. The risk of vertical transmission increases with higher maternal viraemia and human immuno-deficiency virus (HIV) co-infection but current international guidelines do not suggest avoidance of vaginal delivery and breastfeeding to minimise the risk of vertical transmission. The diagnosis of perinatal transmission is different from that in older child or adult and detection of HCV-RNA is essential. Although the natural history of HCV infection in children is not well characterised, almost 50-80% will progress to chronic hepatitis among vertically infected and blood transfusion acquired hepatitis C cases. Children have a lower viral load, lower ALT values and milder histological derangement as compared to adults with chronic hepatitis C cases. Experience of treatment of chronic hepatitis C in children is limited and still evolving. Few patients achieve spontaneous remission and progression to a more severe liver disease might occur in adult life. Here, the natural history, diagnosis and management of HCV infection in children are discussed with special emphasis on features which are different from adults.     

贵州地区丙型肝炎病毒基因亚型分布状态

目的:探讨贵州地区丙型肝炎病毒(HCV)基因亚型分布状态.方法:在164份抗HCV抗体和HCVRNA均阳性的血清标本中,分别提取HCV RNA,通过逆转录巢式PCR(RT nested-PCR)扩增C基因的羧基端至E1基因的氨基端长度为474 bp的片段,测定其核苷酸序列,与GenBank中已知的HCV序列进行系谱分析,确定HCV基因亚型.结果:164份HCV感染者血清标本通过RT-nested均获得阳性条带,特异性和敏感性均较好,序列与系谱分析显示1a3例(1.8％)、1b 58例(35.4％)、2a 2例(1.2％)、3a 25例(15.2％)、3b 38例(23.2％)及6a 35例(21.3％).结论:贵州地区HCV流行的基因亚型有1a,1b,2a,3a,3b,6a共6种,主要为1b、3a、3b和6a亚型,提示贵州地区HCV流行的基因亚型呈现多样性.     

Hepatitis C and diabetes mellitus

Hepatitis C virus infection in diabetes mellitus is more common than in non-diabetic population. Earlier it was thought to be due to more use of needles for insulin injections and frequent blood examination which has been recently antagonised by recent studies. Hepatitis C virus infection has shown to produce insulin resistance (because of liberated cytokines) insulin secretory defect (by viral infection or auto-immune damage). Hepatitis C virus infection also leads to non-alcoholic fatty liver disease (a probable component of insulin resistance syndrome) and increased iron increased iron storage in the body. All these factors may explain hepatitic C virus infection as an aetiology for diabetes mellitus. If future researches strongly establish this fact, antiviral or vaccines for hepatitis C virus infection should be thought of for preventing diabetes mellitus.     

丙型肝炎治疗的研究进展

丙型肝炎严重威胁着人类的健康,目前寻找一种有效的疗法至关重要。撰文对丙型肝炎的药物治疗、RNA干扰、病毒抗原编码基因的转基因表达、反义核酸技术及表位疫苗等项治疗方案予以综述,提出了包含有多个保守丙型肝炎病毒(HCV)抗原表位的多价融合抗原基因的DNA疫苗将成为今后丙型肝炎治疗的研究方向。该疫苗可以在不同个体中激起广泛而强烈的对不同HCV基因型有交叉反应性的T细胞免疫应答,并有望用于丙型肝炎人群的治疗。     

Hepatitis C. An update

Hepatitis C is a long-term viral infection affecting the liver caused by the hepatitis C virus HCV. Hepatitis C can be silent for years before symptoms appear, and liver damage occurs. The hepatitis C virus is extremely infectious, which means that only a tiny amount of HCV can cause illness. Hepatitis C is a major public health problem worldwide with far-reaching implications because of the chronicity of the infection that leads to chronic liver disease, cirrhosis, and primary hepatocellular carcinoma.     

丙型肝炎病毒感染外周血单个核细胞对丙型肝炎的影响

为了研究丙型肝炎病毒(HCV)感染外周血单个核细胞(PBMC)对丙型肝炎的影响,运用非同位素原位杂交法(NISH)和链酶亲和素-生物素(SABC)法分别检测20例慢性丙型肝炎患者PBMC中的HCV-RNA及其T淋巴细胞亚群,同时检测这些患者的肝功能指标。结果显示8例(40．0％)HCV患者的PBMC中的HCV-RNA呈阳性结果。HCV-RNA呈散在颗粒状或弥漫分布,主要位于胞浆中。HCV-RNA阳性组和阴性组的CD+4T细胞比例低于正常对照组,CD+8T细胞比例高于正常对照组,CD+4／CD+8比值下降;而HCV-RNA阳性组的CD+4T细胞比例则又低于阴性组,CD+8T细胞比例高于阴性组,CD+4／CD+8比值出现倒置(P<0．01)。两组的肝功能检查结果之间无显著差异(P>0．05)。提示HCV感染PBMC后引起T淋巴细胞亚群发生变化,使CD+4和CD+8T细胞功能下降或不能很好地协调作用,从而成为HCV持续感染的重要原因之一。HCV感染PBMC对肝脏炎症程度的影响可能不大。     

GBV-C和HCV共同感染的研究

目的：了解GBV-C和HCV的共同感染率,及不同引物和自制DIG标记探针检测GBV-C的效果。方法：定量RT-PCR检测肝炎患者血清标本中的HCV,RT-nested PCR检测HCV RNA阳性标本中的GBV-C,分析部分标本扩增产物的棱苷酸和氨基酸序列,Southern杂交鉴定GBV-C扩增产物的特异性．结果：211例丙型肝炎病人血清标本中,GBV-C 5’-NCR和GBV-CNS3区检出率分别为31．8%和22．8%,总阳性率为35．1％．部分标本扩增产物的核苷酸序列分析证实,RT-nested PCR获得的检测结果可靠,但序列中存在较高频率的随机突变．自制的GBV-C 5‘-NCR和NS3 DIG标记探针有较高的特异性,可用于检测相应的扩增产物。结论：GBV-C 5‘-NCR引物的检测效果优于GBV-C NS3,GBV-C与HCV有较高的共同感染率。     

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     

布朗医生日记——我的六位丙型肝炎患者

病例1 我第一次见到Ginger是在1983年，发现她的肝脏转氨酶升高，我想可能与肝损伤有关。但是过了几年，转氨酶持续升高，对此我感到迷惑，1992年第一代丙肝抗体检测问世，问题就很清楚了，原来他患了丙型肝炎。Ginger是我第一个患有丙型肝炎的病人。她很想知道丙型肝炎是什么，是怎样患上的，可那时我并不很清楚，我们每年都给她复查肝功能，     

丙型病毒性肝炎的研究进展

丙型病毒性肝炎由丙型肝炎病毒（HCV）感染所致.HCV感染呈全球分布,我国是高流行地区,由于HCV基因的高变性,容易逃避机体免疫系统的清除.HCV感染免疫系统细胞,造成机体对HCV感染的免疫应答异常,并引起组织的损伤,导致肝细胞的慢性持续性感染,并可进一步发展成肝硬化,甚至肝细胞肝癌.HCV主要经血液传播,包括输血与血制品传播、静脉吸毒、针刺、医源性传播、性接触和母婴垂直传播等.