HCV感染的肝外相关性疾病

丙型肝炎病毒(HCV)感染者呈世界性分布,近年发现HCV感染不但可能感染肝细胞,也可以侵入肝外多种组织和器官,而出现许多肝外相关的疾病。本文对近年来HCV感染的肝外表现作一综述,以引起国内同道们的注意。1 HCV感染性糖尿病国外一项流行病学调查研究发现:慢性丙型肝炎(HCV)患者的糖尿病发病率明显高于其它肝炎病毒感染性慢性肝病者,HCV-CAH的糖尿病发病率达25.5％,HCV性肝硬化时可达38％(对照HBV感染组仅7.8％～12％)。有研究者统计HCV性慢性肝病时糖尿病发病率可达HBV感染组的10倍以上。HCV性     

HBV相关的慢性肝病与胰岛素抵抗的研究进展

肝脏是调节血糖代谢的重要脏器,肝细胞受损时可能出现糖代谢紊乱及胰岛素抵抗(insulin resistance,IR),甚至发展为肝源性糖尿病.目前病毒性肝炎、肝硬化与糖尿病的相关性研究已经成为近年来的热点问题,本文就乙型肝炎病毒(hepatitis B virus,HBV)感染与糖尿病的早期预测指标的研究新进展作一综述,简单介绍了IR的概念及出现的原因,详细阐述了HBV感染、HBV及丙型肝炎病毒重叠感染、肝炎肝硬化与IR的相互联系,并附带介绍了乙型肝炎病毒感染人群出现IR的有关机制.关于IR对HBV相关的慢性肝病患者预后的影响,本文主要阐述的是IR对HBV感染人群出现脂肪肝、肝纤维化、肝癌的影响,该综述还明确讲述了HBV感染并IR人群的临床治疗.     

丙型肝炎病毒感染与脂肪性肝病

HCV除引起肝脏损害外,还与肝细胞癌(HCC)以及某些肝外组织的损害表现密切相关.大量研究报道,HCV慢性感染与2型糖尿病、脂肪肝等代谢性疾病的发生,发展密切相关[1].     

乙型和丙型肝炎病毒蛋白反式激活作用机制及其意义的研究进展

编者按乙型肝炎病毒(HBV)和丙肝炎病毒(HCV)感染不仅引起急性、慢性病毒性肝炎,而且与肝纤维化(LF)、肝细胞癌(HCC)的发生、发展密切相关.     

乙型和丙型肝炎病毒对MAPKK信号转导的影响

0 引言乙型肝炎病毒(HBV)和丙型肝炎病毒(HCV)的感染,不仅引起急、慢性病毒性肝炎,而且与肝纤维化、肝细胞癌的发生密切相关。虽然HBV和HCV感染与肝细胞癌之间的关系已经得到确定,但是具体的分子生物     

慢性丙型肝炎与糖尿病的相关性

慢性丙型肝炎(CHC)是由丙型肝炎病毒(HCV)感染引起的一种慢性感染性肝脏疾病[1].HCV是一种RNA病毒,与乙型肝炎病毒(HBV)这种DNA病毒的致病机制不同.目前已经积累的临床与研究资料表明,慢性HCV感染不仅引起CHC、肝硬化、肝细胞癌,而且还引起一系列的全身性的代谢疾病,我们曾经提出HCV感染引起的多代谢综合征(metabolicdisturbance syndrome))的概念[2].近年来的研究资料表明,HCV感染可以引起2型糖尿病(NIDDM)的发生[3].     

慢性丙型肝炎与代谢综合征

丙型肝炎病毒感染除引起肝脏损害、肝细胞癌(hepatocellular carcinoma,HCC)有相关性之外,还与肝外组织的损害表现密切相关.国内外研究证实慢性丙型肝炎发病机制之一是肝脏脂肪变性,提示是一种代谢性疾病,丙型肝炎病毒与代谢综合征(metabolic syndrome,MS)密切相关,肝脏脂肪变性及胰岛素抵抗可能是丙型肝炎病毒致代谢综合征的中心环节,其分子生物机制可能是病毒致脂代谢紊乱,但是其更加深入而确切的机制仍不完全知晓,还有待深入研究.     

乙型肝炎病毒和丙型肝炎病毒蛋白对亮氨酸拉链蛋白LZIP的调节

0 引言乙型肝炎病毒(HBV)和丙型肝炎病毒(HCV)的感染,不仅引起急、慢性病毒性肝炎,而且与肝纤维化、肝细胞癌(HCC)的发生密切相关.虽然HBV、HCV感染与肝细胞癌之间的关系已经得到确定,但是具体的分子生物学机制还有许多工作要做.其中肝炎病毒编码蛋白对于肝细胞基因组表达的反式调节作用,即肝炎病毒蛋白与肝细胞基因组启动子DNA结合,对于肝细胞基因表达谱产生影响,从而调节肝细胞的生长、代谢、凋亡及恶性转化,在病毒感染致病机制中起着重要作     

HBV/HCV重叠感染的抗病毒治疗

从全球范围看,乙型肝炎病毒(hepatitis B virus,HBV)和丙型肝炎病毒(hepatitis C virus,HCV)重叠感染估计约有700-2000万人口感染.重叠感染和单一HBV或HCV感染比较,更易发展为肝硬化、肝细胞癌甚至肝衰竭的比例也高,HBV和HCV重叠感染可有四种不同的临床模式,即HCV活动...     

HCV HBV感染与肝细胞性肝癌

调查了肝癌高发地区不同肝病患者中丙型肝炎病毒(HCV)感染率。慢性肝病患者绝大多数已被乙型肝炎病毒(HBV)感染。HCV第二代抗体阳性率,肝癌7.3％,肝硬化6.6％,慢性肝炎6.6％和急性肝炎3.4％。两种病毒的复合感染率,肝癌5.1％,肝硬化1.7％,慢性肝炎3.9％和急性肝炎1.1％。在38例HCV抗体阳性的慢性肝病患者中,ALT异常84.2％,有输血史者占57.9％,HCV-RNA阳性率为71.1％。本研究的资料分析提示,在肝癌高发地区尽管HCV抗体阳性率较低,但HCV感染也是肝癌发生的重要病因之一。     

MiR-122 in hepatitis B virus and hepatitis C virus dual infection

Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are the most common causes of chronic liver diseases and hepatocelluar carcinomas. Over the past few years, the liver-enriched microRNA-122 (miR-122) has been shown to differentially regulate viral replication of HBV and HCV. It is notable that the level of miR-122 is positively and negatively regulated by HCV and HBV, respectively. Consistent with the well-documented phenomenon that miR-122 promotes HCV accumulation, inhibition of miR-122 has been shown as an effective therapy for the treatment of HCV infection in both chimpanzees and humans. On the other hand, miR-122 is also known to block HBV replication, and HBV has recently been shown to inhibit miR-122 expression; such a reciprocal inhibition between miR-122 and HBV suggests an intriguing possibility that miR-122 replacement may represent a potential therapy for treatment of HBV infection. As HBV and HCV have shared transmission routes, dual infection is not an uncommon scenario, which is associated with more advanced liver disease than either HBV or HCV mono-infection. Thus, there is a clear need to further understand the interaction between HBV and HCV and to delineate the role of miR-122 in HBV/HCV dual infection in order to devise effective therapy. This review summarizes the current understanding of HBV/HCV dual infection, focusing on the pathobiological role and therapeutic potential of miR-122.     

慢性肝病者乙型和丙型肝炎病毒重叠感染的研究

对２１３例老年慢性肝病患者的乙型肝炎病毒（ＨＢＶ）和丙型肝炎病毒（ＨＣＶ）血清标志物检测发现：ＨＢＶ感染占７３．２４％、ＨＢＶ和ＨＣＶ重叠感染占重叠感染点１５．４９％、ＨＣＶ感染占７．０４％、其它占４．２６％；ＨＢＶ阴性者ＨＣＶ检出率高于ＨＢＶ阳性者，肝癌和肝硬化患者较慢性肝炎患者高；ＨＢＶ和ＨＣＶ重叠感染患者的血清血蛋白下降显著，γ－球蛋白升高明显，肝硬化并腹水和上消化道出血者了多。结果表明，老     

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Concurrent hepatitis C virus (HCV), hepatitis delta virus (HDV), or human immunodeficiency virus (HIV) infection with chronic hepatitis B virus (HBV) appears to increase the risk of progressive liver disease including liver cirrhosis and hepatocellular carcinoma. There is a 10% prevalence of HCV infection in chronic HBV or HDV infection. Serological evidence of previous exposure to HBV is found in more than 80% of HIV-positive patients in the high risk group. Notably, the most recently acquired virus tends to suppress the pre-existing virus. In chronic HBV infection acquired perinatally or in early childhood, usually HCV is dominant and may suppress or even displace HBV and HDV. Less frequently, HBV or HDV suppresses HCV. It is generally agreed that the dominant virus should be identified in order to make appropriate treatment decisions. Studies with standard interferon (IFN) to treat patients with HCV dominantly dual HBV/HCV infection have showed only limited virological response. But high dose of IFN has been demonstrated with better response rate. Combined ribavirin with standard or pegylated IFN therapy could achieve a sustained HCV clearance rate comparable with those infected with HCV alone. On the contrary, patients with HBV dominantly dual viral infection might indicate more appropriate addition of lamivudine to IFN than ribavirin. Additionally, patients with concurrent infection of HBV and HDV, IFN seems to be the only effective agent. However, the efficacy of IFN is related to the dose. High dose of IFN [9 MU tiw (thrice per week)] and longer treatment duration (at least 2 years) have been shown to achieve adequate virological response. In patients with concurrently infected HBV and HIV, anti-HBV therapy should be considered for all patients with evidence of liver disease, irrespective of the CD4 cell count. In patients not requiring antiretroviral therapy, HBV therapy should be preferentially based on IFN, adefovir, or telbivudine. In contrast, in patients with CD4 cell counts <350 cells/μl or those already on antiretroviral therapy, agents with double anti-HBV and anti-HIV activity are preferred. At present, the evidence of therapeutic efficacy is not sufficient to make a recommendation in treating patients with dual HBV/HCV or HBV/HDV or HBV/HIV infection. Further studies of the well-designed, larger scale are needed to elucidate the role of different regimens or combination in the treatment of dual viral infection.     

Nucleoporin 88 expression in hepatitis B and C virus-related liver diseases

INTRODUCTIONHepatocellular carcinoma (HCC) ranks fifth of the most common cancers worldwide and its incidence is rising in the Western world[1]. Due to the high mortality associated with HCC it is the third leading cause of cancer death worldwide[1]. The …     

Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma

Chronic infection with viral hepatitis affects half a billion individuals worldwide and can lead to cirrhosis, cancer, and liver failure. Liver cancer is the third leading cause of cancer-associated mortality, of which hepatocellular carcinoma (HCC)represents 90%of all primary liver cancers. Solid tumors like HCC are complex and have heterogeneous tumor genomic profiles contributing to complexity in diagnosis and management. Chronic infection with hepatitis B virus (HBV),hepatitis delta virus (HDV), and hepatitis C virus (HCV) are the greatest etiological risk factors for HCC. Due to the significant role of chronic viral infection in HCC development, it is important to investigate direct (viral associated) and indirect (immune-associated) mechanisms involved in the pathogenesis of HCC. Common mechanisms used by HBV, HCV, and HDV that drive hepatocarcinogenesis include persistent liver inflammation with an impaired antiviral immune response, immune and viral protein-mediated oxidative stress, and deregulation of cellular signaling pathways by viral proteins.DNA integration to promote genome instability is a feature of HBV infection, and metabolic reprogramming leading to steatosis is driven by HCV infection. The current review aims to provide a brief overview of HBV, HCV and HDV molecular biology, and highlight specific viral-associated oncogenic mechanisms and common molecular pathways deregulated in HCC, and current as well as emerging treatments for HCC.     

Occult hepatitis B virus infection is not associated with disease progression of chronic hepatitis C virus infection

AIM To clarify the prevalence of occult hepatitis B virus(HBV) infection(OBI) and the association between OBI and liver disease progression, defined as development of liver cirrhosis or hepatocellular carcinoma(HCC), worsening of Child-Pugh class, or mortality in cases of chronic hepatitis C virus(HCV) infection. METHODS This prospective cohort study enrolled 174 patients with chronic HCV infection(chronic hepatitis, n = 83; cirrhosis, n = 47; HCC, n = 44), and evaluated disease progression during a mean follow-up of 38.7 mo. OBI was defined as HBV DNA positivity in 2 or moredifferent viral genomic regions by nested polymerase chain reaction using 4 sets of primers in the S, C, P and X open reading frame of the HBV genome. RESULTS The overall OBI prevalence in chronic HCV patients at enrollment was 18.4%, with 16.9%, 25.5% and 13.6% in the chronic hepatitis C, liver cirrhosis and HCC groups, respectively(P = 0.845). During follow-up, 52 patients showed disease progression, which was independently associated with aspartate aminotransferase 40 IU/L, Child-Pugh score and sustained virologic response(SVR), but not with OBI positivity. In 136 patients who were not in the SVR state during the study period, OBI positivity was associated with neither disease progression, nor HCC development. CONCLUSION The prevalence of OBI in chronic HCV patients was 18.4%, and OBI was not associated with disease progression in South Koreans.     

庚型肝炎病毒感染的临床流行情况和致病力的探讨

目的：为了弄清肝病患者中庚型肝炎病毒（ＨＧＶ）的临床感染情况和评估庚型肝炎病毒的致病力。方法：本文调查了２１３例肝病患者的ＨＧＶ感染情况和分析了ＨＧＶ感染的致病力。结果：在２１３例肝病患者中，ＨＧＶ的感染率为７５％（１６／２１３）；其中，ＨＧＶ与ＨＢＶ、ＨＣＶ以及ＨＢＶ和ＨＣＶ的合并感染分别是为７１％（９／１２７）、１８２％（２／１１）和２７８％（５／１８）。未发现ＨＢＶ合并ＨＧＶ感染和单独ＨＢＶ感染两组之间肝功能的损害程度存在差异。结论：以上结果提示，ＨＧＶ通常与胃肠外传播的ＨＢＶ和ＨＣＶ合并感染。而且，ＨＧＶ的致病力看来是温和的