山东地区丙型肝炎病毒的基因型及血清学分型的研究

探索山东地区丙型肝炎病毒(HCV)的基因型及血清学分型的分布,了解HCV基因型与感染途径的关系.对96例抗HCV阳性患者的血清进行HCV RNA检测,HCV RNA阳性者,应用限制性片段长度多态性分析(RELP)进行基因分型;同时应用Murex Serotyping HCV 1-6血清学分型试剂进行血清学分型.基因非2(1b)型79例,占83.16%,2(2a)型为16例占16.84%,44份血清标本的血清学分型可分型率为90.91%,与基因分型的符合率为90.00%.不同的感染途径之间,基因型分布没有差异(P=0.15).山东地区丙型肝炎病毒流行株为基因非2(1b)和2(2a)型,非2(1b)型为优势株,基因分型与血清学分型结果基本一致,基因型与丙型肝炎的感染途径无关.     

天津市慢性丙型肝炎患者感染途径分析

目的 分析天津市133例慢性丙型肝炎(丙肝)患者的感染途径,为丙肝的预防提供依据.方法 2009 ～2012年天津市133例确诊为慢性丙型肝炎患者,通过患者的主诉确定丙肝的感染途径.采用FQ-PCR技术检测血清HCV RNA定量,对于HCV RNA定量＞1 000 IU/mL者参照文献采用基因芯片行HCV RNA基因型检测.应用全自动生化分析仪检测肝功能.结果 133例慢性丙肝患者感染途径有输血及血制品76例,手术10例,牙齿治疗13例,穿耳洞、纹身13例,母婴传播1例,吸毒5例,不明原因15例.38例患者进行病毒基因型检测,1b型患者32例,2a型患者5例,3型患者1例.其中1b型患者输血或血制品感染18例,2a型患者输血或血制品感染4例.2000年之前经输血或血制品感染丙肝的感染率(84.1％)显著高于2000年及之后感染者(23.1％),P＜0.01(x2=30.70),而2000年及之后感染者多数是经纹身、穿耳洞、吸毒等不良生活方式感染.输血及血制品感染者与非输血感染者的年龄分别为(53.84±10.94)、(42.70±12.71)岁,白蛋白(ALB)水平分别为(37.08±6.68)、(41.10 ±5.18) g/L,两者比较,P均＜0.01;病毒载量、丙氨酸氨基转氨酶(ALT)、总胆红素(TBIL)、甲胎蛋白(AFP)三指标在两者之间无统计学差异.不同年龄段慢性丙肝患者血清学指标比较,P均＞0.05.结论 HCV感染者的感染途径包括经输血及血制品途径及经纹身、牙齿治疗、吸毒等非输血途径,病毒基因型多数为1b和2a型,对目前丙肝的主要感染途径进行有效阻断是防止丙肝感染的重要途径.     

长春地区出入境人员感染丙型肝炎病毒的基因分型研究

目的研究长春地区出入境人员感染丙型肝炎病毒(HCV)的基因型分布。方法收集42例丙型肝炎阳性者的血清标本,采用基因测序法进行HCV基因型检测和分析。结果 42份HCV阳性血清基因分型分别为1b、1a、2a,其中基因1型21份(占50%),1b亚型13份(占30.95%),1a亚型8份,2a亚型9份。HCV基因型性别、年龄分布差异无统计学意义(P0.05)。结论长春地区出入境人员感染的HCV以1b型为主,2a型次之。     

上海地区71例慢性丙型病毒性肝炎患者基因型分布研究

目的：观察上海地区慢性丙型肝炎（慢丙肝）患者的丙肝病毒（HCV）基因型分布情况。方法：提取血清HCVRNA，套式PCR扩增方法扩增目的片段，纯化后直接测序。结果：71例血清标本检测示，1b型占87．32％（62／71），2a型占12．68％（9／71），共有22个突变。1b型的突变率为33．87％（21／62），2a型的突变率为11．11％（1／9）。两种基因型突变率比较，具统计学差异（P〈0．05）。结论：该研究中HCV基因型为1b和2a两型。1b型占多数，1b型的突变率高于2a型。     

中国东北丙型肝炎病毒感染基因特征及人群易感性分析

采用微板核酸杂交-ELISA法及基因芯片技术对5 79例HCV感染者的HCV基因型以及30例HCV感染者以及30例健康人HLA -DRB1等位基因分布情况进行分析,探讨中国东北丙型肝炎病毒(HCV)感染基因型特征及丙型肝炎病毒感染的人群易感性。5. 79例患者中Ⅳ/ 2b型HCV感染率最高,为5 1 .12 % ;约34 .72 %的HCV感染者ALT持续正常;Ⅱ/ 1b型和混合型HCV感染在ALT反复升高组中的感染率明显高于ALT持续正常组(P <0 .0 5 )。Ⅰ型和Ⅲ型HCV合并HBV感染的发生率较高,混合型HCV合并HBV感染的发生率较低,与单独感染比较差异显著(P <0 .0 5 ) ;混合型HCV感染主要见于有2次或2次以上输血史者。HLA -DRB1 0 4和DRB1 13在HCV感染者中的出现频率较高,与健康对照组相比差异显著(P <0. 0 5 )。因此,中国东北地区HCV感染以Ⅳ/ 2b型为主,约34 72 %的HCV感染者不表现出肝炎的症状,可能成为重要的传染源。Ⅱ/ 1b型和混合型HCV感染更容易导致肝细胞损伤。Ⅰ/ 1a型和Ⅲ/ 2a型HCV可能更易于同HBV共存,两种或两种以上基因型共存的HCV则不易于同HBV合并感染。反复接受血液或血制品可能是出现混合型HCV感染的主要原因。HLA -DRB1 0 4和DRB1 13等位基因可能与HCV的人群易感性有关。     

长春地区丙型肝炎病毒基因分析

目的了解长春地区HCV基因分型情况，为HCV感染者的诊断和治疗提供重要的科学依据。方法荧光定量RT-PCR检测97例抗-HCV阳性血清标本，并对89例HCV-RNA阳性的血清标本应用基因芯片法进行HCV基因分型。结果89例阳性标本中HCV1b型49例，HCV2a型37例，HCV1b／2a混合型3例。结论长春地区HCV基因型主要为1b型，2a型次之，同时存在HCV1b／2a混合型。     

慢性丙型肝炎患者HCV基因型分析

目的研究慢性丙型肝炎患者HCV基因型概况。方法采用基因芯片法检测HCV基因分型;采用PCR法测定HCV RNA定量。结果在570例患者中,HCV RNA阳性552例（95%）,其中1b型400例（72.4%）,2a型63例（11.4%）,3a型20例（3.6%）,3b型20例（3.6%）,1b＋2a型12例（2.1%）,1a型2例（0.4%）,6型7例（1.26%）,1b＋3a型1例（0.18%）,2a＋1b型3例（0.5%）,未定型24例（4.3%）;不同HCV基因型感染者血清HCVRNA水平无统计学差异（P〉0.05）。结论本组患者HCV基因型以1b型为主,2a型次之,多种混合型的出现提示HCV基因型呈现多样化趋势。     

太原地区丙型肝炎病毒基因分型及其临床意义

目的了解本地区HCV基因型分布,探讨HCV基因分型的临床意义。方法用RT-nested-PCR方法扩增62例丙型肝炎患者血清HCV5’ UTR区,限制性内切酶HaeⅢ、Bsh1236Ⅰ进行双酶切得到不同长度基因片段,分析结果,确定基因型。结果62例丙型肝炎患者中,其中1b型43例,2a型9例,1b/2a混合型5例,1a型1例,3a型1例,未分型3例。基因1b型患者肝功能、肝脏脂肪变性均较非1b型严重。结论本地区丙型肝炎以基因1b型为主,且该型患者临床病情较其它型严重。     

贵州地区HCV感染者基因型分布特征

目的 探讨贵州地区丙型肝炎患者HCV基因型分布特征,为HCV感染的防控和个体化治疗提供临床依据。方法 选取2011年9月-2018年10月贵阳市公共卫生救治中心1211例HCV RNA阳性的丙型肝炎患者,采用PCR直接测序法,与GenBank中已知的HCV序列进行对比,获得HCV基因型及亚型,并分析其分布与性别、年龄、民族、地区、感染途径等因素的关系。计数资料组间比较采用χ2检验或Fisher确切概率法。结果 1211例HCV感染者共检出4种基因型和11种基因亚型,其中以1b型(26.84%)、3b型(27.17%)和6a型(24.28%)为主。不同HCV基因型在男女感染者中分布差异有统计学意义(χ2=15.428,P=0.009),其中男性以3b型为主(29.34%),女性以1b型为主(32.21%)。不同HCV基因型分布在各年龄组中差异有统计学意义(χ2=67.439,P<0.001),≤18岁组与≥60岁组以1b型为主(分别为66.67%、58.93%),而19~39岁组以3b型(28.93%)、6型(29.29%)为主,40~59岁组以1b型(29.54%)、3b型(27.33%)和6型(24.28%)为主。各种感染途径的HCV基因型分布差异有统计学意义(χ2=153.916,P<0.001),感染方式以静脉药瘾为主(57.97%),其次是性接触和有创美容(均为8.42%);经静脉药瘾、有创美容感染HCV者均以3b型为主(分别为31.48%、32.35%),性接触感染者多为HCV 6型(36.27%)。不同民族、贵州地区间HCV基因型分布差异均无统计学意义(P值均>0.05)。结论 贵州地区HCV基因型分布呈多样性,3b、1b、6a型为主要流行株,存在HCV 6型中的多种少见基因亚型,且在不同的年龄、性别、感染途径方面HCV基因型分布存在差异。     

特殊人群的丙型肝炎特点及处理

1 儿童丙型肝炎1.1 流行病学我国健康体检儿童HCV感染率约为0.7%, 曾多次接受输血的患儿HCV感染率可达到22.9%.近年来根据国内存在的HCV基因型研究报道,发现常见的基因型为1-3型.目前认为感染我国人群的HCV主要是1b/Ⅱ型和2a/Ⅲ型,1a/Ⅰ型和2b/Ⅳ型少见.香港越南尚有基因6型发现. 台湾8例手术后发生的慢性丙型肝炎病儿中的4例呈现持续性的病毒复制,但没有肝炎的临床表现.另3 例有病毒血症和慢性肝炎.5例病儿的HCV基因型为2     

Hepatitis C virus (HCV) genotypes in Spanish patients with HCV infection: relationship between HCV genotype 1b, cirrhosis and hepatocellular carcinoma

Background/Aims: The influence of the infecting virus genotype on the progression of the underlying liver disease in patients with chronic hepatitis C virus (HCV) infection remains controversial. The aim of this study was to investigate the prevalence of HCV genotypes in Spanish patients with chronic HCV infection and to elucidate the relationship between the infecting genotype and severity of the disease.Methods: A cross-sectional, retrospective analysis of frequency distribution of HCV genotypes was carried out in 414 Spanish patients with chronic HCV infection, including 243 patients with asymptomatic or minimally symptomatic chronic hepatitis, 112 patients with cirrhosis and hepatocellular carcinoma and 59 patients with decompensated cirrhosis. HCV genotype was determined by restriction fragment length polymorphisms of the 5′ non-coding region.Results: Infection with HCV genotype 1b was found in 72% of patients with chronic hepatitis and in more than 90% of patients with cirrhosis, with or without hepatocellular carcinoma. Older age, infection with genotype 1b and absence of overt parenteral exposure as a possible source of infection were associated with cirrhosis and hepatocellular carcinoma by univariate analysis and this association was confirmed by regression analysis.Conclusions: HCV genotype 1b is associated with advanced liver disease in our geographical area. However, this may be related to a cohort-effect caused by over-representation of genotype 1b in older patients with more advanced disease, because, in our country, this HCV genotype appeared earlier in time and is therefore associated with more prolonged periods of infection.     

慢性丙型肝炎患者糖尿病并发率调查及其临床特征分析

探讨慢性丙型肝炎病毒(HCV)感染与Ⅱ型糖尿病发病的关系。随机选取134例慢性丙型肝炎患者(并发肝硬化者36例)和237例慢性乙型肝炎患者(并发肝硬化者92例),将其分为肝炎组和肝硬化组进行对照分析。此外还随机选取140例Ⅱ型糖尿病患者和203例常规体检人群检测HCV感染状况。134例丙型肝炎患者合并Ⅱ型糖尿病者27例(20．15%),明显高于对照组慢性乙型肝炎患者的8．86%;而且HCV感染病程越长、年龄越大者Ⅱ型糖尿病并发率越高;有糖尿病家族史的HCV感染者并发糖尿病的机率明显高于无糖尿病家族史者。HCV感染者Ⅱ型糖尿病并发率明显高于对照组慢性HBV感染者,其中合并肝硬化者并发率更高;Ⅱ型糖尿病的患者HCV感染的几率也明显增高。     

New perspectives in occult hepatitis C virus infection

Occult hepatitis C virus (HCV) infection, defined as the presence of HCV RNA in liver and in peripheral blood mononuclear cells (PBMCs) in the absence of detectable viral RNA in serum by standard assays, can be found in anti-HCV positive patients with normal serum levels of liver enzymes and in anti-HCV negative patients with persistently elevated liver enzymes of unknown etiology. Occult HCV infection is distributed worldwide and all HCV genotypes seem to be involved in this infection. Occult hepatitis C has been found not only in anti-HCV positive subjects with normal values of liver enzymes or in chronic hepatitis of unknown origin but also in several groups at risk for HCV infection such as hemodialysis patients or family members of patients with occult HCV. This occult infection has been reported also in healthy populations without evidence of liver disease. Occult HCV infection seems to be less aggressive than chronic hepatitis C although patients affected by occult HCV may develop liver cirrhosis and even hepatocellular carcinoma. Thus, anti-HCV negative patients with occult HCV may benefit from antiviral therapy with pegylated-interferon plus ribavirin. The persistence of very low levels of HCV RNA in serum and in PBMCs, along with the maintenance of specific T-cell responses against HCV-antigens observed during a long-term follow-up of patients with occult hepatitis C, indicate that occult HCV is a persistent infection that is not spontaneously eradicated. This is an updated report on diagnosis, epidemiology and clinical implications of occult HCV with special emphasis on anti-HCV negative cases.     

Genotypes of hepatitis C virus in Guangxi Province, southern China

Abstract Hepatitis C virus (HCV) has been subdivided into at least four genotypes, and the prevalence of each genotype has been reported to differ widely in different countries. Of 304 patients with chronic liver diseases (68 with chronic hepatitis, 50 with liver cirrhosis and 186 with hepatocellular carcinoma) from Guangxi Province in southern China, only 9 (3.0%) had antibodies to HCV as determined by a second-generation enzyme immunoassay with a cut-off index of 2.0 or more. The HCV genotypes of these nine cases were examined using polymerase chain reaction with type-specific primers deduced from putative core gene. Seven of the nine cases had type II infection and the other two cases showed double infection with types II and IV. These findings indicate that the predominant HCV genotype in the Guangxi area is type II, as is the case in Japan, although the prevalence of HCV infection in patients with chronic liver diseases is much lower.     

Prevalence of antibodies to hepatitis C virus among Saudi patients with chronic liver diseases.

The prevalence of antibodies against hepatitis C virus (anti-HCV) was determined in 55 patients with chronic liver diseases including liver cirrhosis (42 patients), liver cirrhosis and hepatocellular carcinoma (8 patients), and chronic active hepatitis (4 patients). A total of 63.6% of these patients were positive for anti-HCV, a significantly higher prevalence than the rate of 3.9% observed in 488 asymptomatic volunteers. Of the 42 patients with liver cirrhosis 16 (38.1%) had positive anti-HCV without any markers of hepatitis B virus (HBV), while 12 (28.6%) had markers of neither HCV nor HBV infection. Our findings suggest that HCV infection may play a significant role in the pathogenesis of chronic liver disease in Saudi Arabia, which is an area of endemic HBV infection. Screening for anti HCV should be considered mandatory in patients with chronic liver disease (CLD) especially where the etiology appears obscure.     

Prevalence of hepatitis C virus antibodies in chronic liver disease and hepatocellular carcinoma patients in India

The prevalence of antibodies to hepatitis C virus (HCV) was investigated in 129 patients with chronic liver disease (85 with chronic active hepatitis and 44 with cirrhosis) and 53 patients with hepatocellular carcinoma. The commercially available second generation anti-HCV enzyme immunoassay kit was used. Antibodies to hepatitis C virus were detected in 16.2% of the patients with chronic liver disease and in 15.1% with hepatocellular carcinoma. Of the HCV positive patients in all groups 51.7% were positive for hepatitis B virus (HBV) markers indicating present or past infection. Prevalence of HBV markers in all the three groups (CAH, cirrhosis and HCC) was higher as compared with anti-HCV prevalence. These results suggest that HCV infection may not be a major cause of chronic liver disease and hepatocellular carcinoma in India and indicate the presence of other aetiological agents.     

Liver transplantation for acute or chronic liver failure by hepatitis non-A, non-B and hepatitis C viral infections: a postoperative follow-up.

Orthotopic liver transplantation (OLT) was performed for liver failure related to hepatitis non-A, non-B (HNANB) or hepatitis C (HCV) infections in 12 patients. Of those, 8 patients had chronic and 4 acute hepatic failure. To determine the incidence of recurrent infection, the clinical course, histological findings and serological HCV markers (HCV-RNA and detection of anti HCV antibodies, respectively) were comparatively studied in these patients. Recurrent infection was apparent in 5 of 6 patients transplanted for liver cirrhosis attributable to chronic HCV infection and with HCV-RNA detectable in serum. The clinical course of infection after OLT varied considerably. Chronic active hepatitis, progressing to liver cirrhosis 13 months postoperatively and an acute hepatitis, resolving spontaneously were seen in one case each. Recurrent infection led to chronic persistent hepatitis in the remainder. None of the patients with acute liver failure experienced recurrent infection. HCV-RNA was detectable in all the patients after OLT, with HCV-RNA present pretransplant, however the presence of HCV-RNA in serum was not necessarily associated with clinical illness.     

Prevalence of antibodies to hepatitis C virus among patients with cryptogenic chronic hepatitis and cirrhosis.

Many cases of chronic hepatitis and cirrhosis cannot be attributed to a known cause and are collectively referred to as cryptogenic chronic liver disease. We have evaluated the role of the hepatitis C virus in the pathogenesis of this condition in a retrospective serum analysis for antibody to hepatitis C virus in 129 patients with cryptogenic liver disease. Other causes of chronic hepatitis and cirrhosis were ruled out by clinical, serum biochemical and serological techniques. All 129 patients were HBcAg negative, but 28 (22%) had antibody to HBcAg. Sera were tested by radioimmunoassays using recombinant peptides for antibodies to nonstructural (C100-3 and C33c) and structural regions (C22) of HCV. Among the 129 patients, 61 (47%) had antibody to C100-3, 76 (59%) had antibody to C33c and 74 (57%) had antibody to C22. Seventy-nine (61%) were reactive with at least one and 76 (59%) were reactive with at least two HCV peptides (this is the criterion used for hepatitis C virus antibody reactivity). A proportion of patients with chronic hepatitis and cirrhosis (55 of 91; 60%) similar to that of patients without cirrhosis (21 of 38; 55%) had hepatitis C virus antibody. No significant clinical, serum biochemical or histological differences were noted between the group of patients with hepatitis C virus antibody and those without this antibody reactivity. Thus more than half the patients with cryptogenic chronic liver disease had hepatitis C virus antibody, suggesting that chronic HCV infection plays a major role in the origin of cryptogenic chronic hepatitis and cirrhosis.     

Long-term treatment of chronic hepatitis C with ursodeoxycholic acid: influence of HCV genotypes and severity of liver disease.

AIMS/BACKGROUND: Current therapy for chronic hepatitis C virus (HCV) infection is based on the administration of interferon alpha (IFN) alone or in combination with other anti-viral agents. However, such therapy is effective in only a minority of selected patients. Long-term ursodeoxycholic acid (UDCA) treatment has been reported to improve liver function and structure especially in cholestatic disorders. We investigated the effect of long-term UDCA treatment on liver function in respect to the severity of chronic liver disease and HCV genotypes. METHODS: Forty-five patients with non-cholestatic laparoscopy-biopsy proven HCV-associated chronic hepatitis (n=16) or cirrhosis (n=29) who had not responded to, or were unsuitable for IFN, were randomly assigned to receive UDCA (600 mg/day; n=23) or no therapy (n=22) for 12 months. At entry, all patients were evaluated by means of conventional and quantitative liver function tests (LFTs), including galactose elimination capacity and antipyrine clearance, HCV antibodies, HCV-RNA and HCV genotypes. LFTs were measured at 6 and at 12 months, whereas HCV-RNA was determined again after treatment. RESULTS: Baseline characteristics were comparable in the two study groups. Long-term UDCA therapy was well tolerated. Based on the analysis of variance, there was a significant decrease in serum transaminase, LDH and GGT levels in UDCA treated patients. By contrast, the activities of these enzymes increased in untreated patients, with AST levels reaching statistical significance only. Statistical analysis also showed that the improvement in biochemical markers was more pronounced in UDCA treated patients with liver cirrhosis than in those with chronic hepatitis but was similar in patients with HCV genotype 1b and non-1b. However, HCV-RNA was positive in all patients after treatment. Quantitative LFTs remained, on average, stable over the 12 months of the trial in all groups. CONCLUSIONS: Long-term UDCA treatment is well tolerated in patients with HCV-associated chronic liver disease. The effect appears to be greater in cirrhotics than in patients with chronic hepatitis but is independent of HCV genotypes. Thus, long-term UDCA treatment, despite the absence of an anti-viral effect, seems beneficial in reducing disease activity in patients with chronic hepatitis or cirrhosis who are unsuitable for IFN therapy.