检索结果-南通市图书馆

Steatosis and insulin resistance in hepatitis C: A way out for the virus?

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2009年第40期15卷 5014-5019页

作者： José A Del Campo Manuel Romero-Gómez Unit for The Clinical Management of Digestive Diseases and CIBERehd Hospital Universitario de Valme

The hepatitis C virus (HCV) induces lipid accumulation in vitro and in vivo. The pathogenesis of steatosis is due to both viral and host factors. Viral steatosis is mostly reported in patients with genotype 3a, whereas meta-bolic steatosis is often associated with genotype 1 and metabolic syndrome. Several molecular mechanisms responsible for steatosis have been associated with the HCV core protein, which is able to induce gene expres-sion and activity of sterol regulatory element binding protein 1 (SREBP1) and peroxisome proliferator-activat-ed receptor γ (PPARγ), increasing the transcription of genes involved in hepatic fatty acid synthesis. Steatosis has been also implicated in viral replication. In infected cells, HCV core protein is targeted to lipid droplets which serve as intracellular storage organelles. These studies have shown that lipid droplets are essential for virus assembly. Thus, HCV promotes steatosis as an eff icient mechanism for stable viral replication. Chronic HCV in-fection can also induce insulin resistance. In patients with HCV, insulin resistance is more strongly associated with viral load than visceral obesity. HCV seems to lead to insulin resistance through interference of intracellular insulin signalling by HCV proteins, mainly, the serine phosphorylation of insulin receptor-1 (IRS-1) and im-pairment of the downstream Akt signalling pathway. The HCV core protein interferes with in vitro insulin signal-ling by genotype-specif ic mechanisms, where the role of suppressor of cytokine signal 7 (SOCS-7) in genotype 3aand mammalian target of rapamycin (mTOR) in geno-type 1 in IRS-1 downregulation play key roles. Steatosis and insulin resistance have been associated with f ibrosis progression and a reduced rate of sustained response to peginterferon plus ribavirin.

关键词： Steatosis Insulin resistance hepatitis cvirus

New combination test for hepatitis C virus genotype and viral load determination using Amplicor GT HCV MONITOR test v2.0

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2005年第4期11卷 469-475页

作者： Motokazu Mukaide Yasuhito Tanaka Hirokazu Kakuda Kei Fujiwara Fuat Kurbanov Eturo Orito Kentaro Yoshioka Kiyotaka Fujise Shoji Harada Takazumi Kozaki Kazuo Takemura Kazumasa Hikiji Masashi Mizokami SRL Inc. 5-6-50ShinmachiHino-shiTokyo 191-0002Japan Department of Clinical Molecular Informative Medicine Nagoya City University Graduate School of Medical Sciences KawasumiMizuhoNagoya 467-8601Japan Department of Internal Medicine and Molecular Science Nagoya City University Graduate School of Medical Sciences KawasumiMizuhoNagoya 467-8601Japan Department of Clinical Molecular Informative Medicine Nagoya City University Graduate School of Medical Sciences KawasumiMizuhoNagoya 467-8601 Japan Third Department of Internal Medicine Nagoya University School of Medicine65 TsurumaShowaNagoya 466-8550Japan Division of Gastroenterology and Hepatology Department of Internal Medicine (Kashiwa) The Jikei University School of Medicine163-1KashiwashitaKashiwaChiba 277-8567Japan SRL Inc. 5-6-50ShinmachiHmo-shiTokyo 191-0002Japan

AIM: To develop a new sensitive and inexpensive hepatitis C virus (HCV) combination test (HCV Guideline test) that enables the determination of HCV genotypes 1, 2 and 3, and simultaneous determination of HCV viral load using commercial Amplicor GT HOV MONITOR test v2.0 (microwell version). METHODS: The HCV Guideline test used the PCR product generated in commercial Amplicor GT HCV Monitor test v2.0 for viral load measurement using microwell plate version of Amplicor HCV Monitor and also captured on separate plates containing capture probes and competitive oligonucleotide probes specific for HCV genotypes 1, 2 and 3, The HCV genotype was subsequently determined using the biotin-labeled PCR product and five biotin-labeled HCV-specific probes. RESULTS: The sensitivity of the HCV Guideline test was 0.5 KIU/mL. Specificity of the HCV Guideline test was confirmed by direct sequencing of HCV core region and molecular evolutionary analyses based on a panel of 31 samples. The comparison of the HCV Guideline test and an in-house HCV core genotyping assay using 252 samples from chronic hepatitis C patients indicated concordant results for 97.2% of samples (59.5% genotype 1, 33.7% genotype 2, 6.0% genotype 3, and 0.8% mixed genotypes). Similarly, the HCV Guideline test showed concordance with a serological test, and the serological test failed to assign any serotype in 12.7% of the samples, indicating a better sensitivity of the HCV Guideline test. CONCLUSION: Clinically, both viral load and genotypes (1, 2 and 3) have been found to be major predictors of antiviral therapy outcome regarding chronic hepatitis C based on guidelines and they are, in normal circumstances, performed as separate stand-alone assays. The HCV Guideline test is a useful method for screening large cohorts in a routine clinical setting for determining the treatment regimen and for predicting the outcome of antiviral therapy of chronic hepatitis C.

关键词： hepatitis cvirus HCV Guideline test Viral Load Genotype

The Prevalence of hepatitis C Virus Infection in Oral Lichen Planus in an Ethnic Chinese Cohort of 232 Patients

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

International Journal of Oral Science 2010年第2期2卷 90-97页

作者： Yu Zhou Lu Jiang Jie Liu Xin Zeng Qian-ming Chen State Key Laboratory of Oral Diseases West China College of Stomatology Sichuan University Chengdu China Section of Oral Biology College of Dentistry the Ohio State University Columbus USA

Aim Oral lichen planush （OLP） is a chronic inflammatory disease, and has been reported to have a correlation with hepatitis cvirus （HCV） infection in some regional investigations. In this study, we investigated the prevalence of HCV in patients with oral lichen planus in an ethnic Chinese cohort. Methodology The antibody of HCV infection was detected by using enzymelinked immunosorbent assay. Moreover, the clinical characteristics of whole the cohort have also been studied, such as the gender, age, clinical type, habits and social factors. Results Of all 232 patients, the antibody of HCV infection was detected positive in 4 patients （1.72%） using enzyme-linked immunosorbent assay. It was lower than that in control group of 2.5%, but not significant （P=0.309）. The positive rate of HCV antibody in the erosive type ones （4.2%） was higher than that in the reticular type ones （1.0%）, but this difference was proved to be not significant （P=0.389）. The clinical characteristics of whole cohort, such as the gender, age, clinical type, habits and social factors, showed the outcome obtained in the present study were similar to thao of our previous study. Conclusion HCV may play no etiological role in oral lichen planus in ethnic Chinese OLP patients.

关键词： hepatitis cvirus oral lichen planus epidemiology Chinese cohort

Transient and etiology-related transcription regulation in cirrhosis prior to hepatocellular carcinoma occurrence

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2009年第3期15卷 300-309页

作者： Frédérique Caillot Céline Derambure Paulette Bioulac-Sage Arnaud Franois Michel Scotte Odile Goria Martine Hiron Maryvonne Daveau Jean-Philippe Salier Inserm Unité 905 and Institut Fédératif de Recherches Multidisciplinaires sur les Peptides Faculté de Médecine-Pharmacie76183 RouenFrance Service d'Anatomie Pathologique Centre Hospitalier Universitaireand Inserm U88933000 BordeauxFrance Département Pathologie Centre Hospitalier Universitaire76183 RouenFrance Service de Chirurgie Générale et Digestive Centre Hospitalier Universitaire76183 RouenFrance Service d'Hépato-gastro-entérologie Centre Hospitalier Universitaire76183 RouenFrance

AIM： To search for transcription dysregulation that could （1） differentiate hepatocellular carcinoma （HCC）-free from HCC-related cirrhosis （2） differentiate HCC-free cirrhosis related to HCV from that related to alcohol intake. METHODS： Using microarray analysis, we compared transcript levels in HCC-free cirrhosis （alcoholism： 7; hepatitis C： 7）, HCC-associated cirrhosis （alcoholism： 10; hepatitis C： 10） and eight control livers. The identified transcripts were validated by qRT-PCR in an independent cohort of 45 samples （20 HCC-free cirrhosis; 15 HCC-associated cirrhosis and 10 control livers）. We also confirmed our results by ***： In HCC-free livers, we identified 70transcripts which differentiated between alcoholicrelated-cirrhosis, HCV-related cirrhosis and control livers. They mainly corresponded to down-regulation. Dysregulation of Signal Transduction and Activator of Transcription-3 （STAT-3） was found along with related changes in STAT-3 targets which occurred in an etiology-dependent fashion in HCC-free cirrhosis. In contrast, in HCC, such transcription dysregulations were not observed. CONCLUSION： We report that transcriptional dysregulations exist in HCC-free cirrhosis, are transiently observed prior to detectable HCC onset and may be appear like markers from cirrhosis to HCC transition.

关键词： Liver Pathology Alcoholism hepatitis cvirus Gene expression Carcinogenesis

Influence of hepatitis viruses on clinico-pathological profiles and long-term outcome in patients undergoing surgery for hepatocellular carcinoma

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Hepatobiliary & Pancreatic Diseases International 2014年第2期13卷 162-172页

作者： Anna-Maria Tanase Traian Dumitrascu Simona Dima Razvan Grigorie Agnes Marchio Pascal Pineau Irinel Popescu Center of General Surgery and Liver Transplant Fundeni Clinical Institute Unité "Organisation nucléaire et oncogenèse" INSERM U993Institut

BACKGROUND: The global risk of hepatocellular carcinoma(HCC) is largely due to hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In recent years, however, an increased prevalence of non-viral HCC has been noted. The clinical impact of the presence/absence of viral infections in HCC remains controversial. The present study aimed to assess the effect of hepatitis viruses on demographics, clinical and pathological features and long-term outcome in a large cohort of Romanian patients who underwent surgery for HCC. METHODS: The study included 404 patients with HCC who had undergone resection, transplantation or radiofrequency ablation at a single institution between 2001 and 2010. The patients were divided into four groups: 85 patients with hepatitis B virus infection (HBV group), 164 patients with hepatitis C virus infection (HCV group), 39 patients with hepatitis B and C virus co-infection (HBCV group), and 116 patients without viral infection (non-BC group). RESULTS: The patients of both HBV (56.0±11.3 years) and HBCV groups (56.0±9.9 years) were significantly younger than those of the HCV (61.0±8.5 years, P=0.001) and non-BC groups(61.0±13.0 years, P=0.002). Interestingly, the prevalence of liver cirrhosis was significantly lower in the non-BC group (47%)than in any other subsets (72%-90%, P<0.002). Furthermore, the non-BC patients were more advanced according to the Barcelona Clinic Liver Cancer stages than the patients of the HCV or HBCV groups (P<0.020); accordingly, they were more frequently assessed beyond the Milan criteria than any other groups (P=0.001). No significant differences in the disease-free or overall survival rates were observed among these groups. CONCLUSIONS: Patients with non-viral HCC are diagnosed at advanced ages and stages, a situation plausibly due to the poor effectiveness of cancer surveillance in community practice. The presence of viral infections does not appear to impair the longterm prognosis after surgical treatm

关键词： hepatitis B virus hepatitis cvirus hepatocellular carcinoma recurrence prognosis

hepatitis C virus genetic variability and evolution

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

World Journal of Hepatology 2015年第6期7卷 831-845页

作者： Natalia Echeverría Gonzalo Moratorio Juan Cristina Pilar Moreno Laboratorio de Virología Molecular Centro de Investigaciones Nucleares Facultad de Ciencias Universidad de la República Viral Populations and Pathogenesis Laboratory Institut Pasteur 75724 Paris CEDEX 15 France Recombinant Proteins Unit Institut Pasteur de Montevideo11400 Montevideo Uruguay

hepatitis C virus(HCV) has infected over 170 million people worldwide and creates a huge disease burden due to chronic, progressive liver disease. HCV is a singlestranded, positive sense, RNA virus, member of the Flaviviridae family. The high error rate of RNA-dependent RNA polymerase and the pressure exerted by the host immune system, has driven the evolution of HCV into 7 different genotypes and more than 67 subtypes. HCV evolves by means of different mechanisms of genetic variation. On the one hand, its high mutation rates generate the production of a large number of different but closely related viral variants during infection, usually referred to as a quasispecies. The great quasispecies variability of HCV has also therapeutic implications since the continuous generation and selection of resistant or fitter variants within the quasispecies spectrum might allow viruses to escape control by antiviral drugs. On the other hand HCV exploits recombination to ensure its survival. This enormous viral diversity together with some host factors has made it difficult to control viral dispersal. Current treatment options involve pegylated interferon-α and ribavirin as dual therapy or in combination with a direct-acting antiviral drug, depending on the country. Despite all the efforts put into antiviral therapy studies, eradication of the virus or the development of a preventive vaccine has been unsuccessful so far. This review focuses on current available data reported to date on the genetic mechanisms driving the molecular evolution of HCV populations and its relation with the antiviral therapies designed to control HCV infection.

关键词： Recombination Quasispecies hepatitis cvirus RNA Evolution Antiviral therapy