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TY - JOUR. T1 - Serum hepatitis C virus RNA level as a predictor of subsequent response to interferon‐α therapy in Japanese patients with chronic hepatitis C. AU - Onto, Etsuro. AU - Mizokami, Masashi. AU - Nakano, Tatsunori. AU - Terashima, Hisahiro. AU - Nojiri, Osamu. AU - Sakakibara, Kenji. AU - Mizuno, Makoto. AU - Ogino, Masataka. AU - Nakamura, Makoto. AU - Matsumoto, Yukoh. AU - Miyata, Ken‐Ichi ‐I. AU - Lau, Johnson Y.N.. PY - 1994/12. Y1 - 1994/12. N2 - Serum hepatitis C virus (HCV) RNA level has been shown to be a good predictor of subsequent response to interferon‐α (IFN) therapy in US patients in whom genotype 1a/1b are both predominant. To determine whether serum HCV RNA level is a predictor of subsequent response to IFN in Japanese patients or not, appropriately collected pre‐IFN therapy serum samples from 35 Japanese patients with chronic HCV infection were studied. Serum HCV RNA level and HCV genotype were determined and correlated with the subsequent response to ...
TY - JOUR. T1 - Mizoribine inhibits hepatitis C virus RNA replication. T2 - Effect of combination with interferon-α. AU - Naka, Kazuhito. AU - Ikeda, Masanori. AU - Abe, Ken Ichi. AU - Dansako, Hiromichi. AU - Kato, Nobuyuki. N1 - Funding Information: We thank T. Nakamura, A. Morishita, and T. Maeta for their helpful experimental assistance. This work was supported by Grants-in-Aid for the third-term comprehensive 10-year strategy for cancer control, and for research on hepatitis from the Ministry of Health, Labor, and Welfare of Japan, and by Grants-in-Aid for scientific research from the Organization for Pharmaceutical Safety and Research (OPSR).. PY - 2005/5/13. Y1 - 2005/5/13. N2 - Interferon (IFN)-α monotherapy, as well as the more effective combination therapy of IFN-α and ribavirin, are currently used for patients with chronic hepatitis C caused by hepatitis C virus (HCV) infection, although the mechanisms of the antiviral effects of these reagents on HCV remain ambiguous, and side ...
Protein target information for Chain A, Hepatitis C Virus Polymerase Ns5b (Bk) With Amide Bioisostere Thumb Site Inhibitor (Hepatitis C virus (isolate BK)). Find diseases associated with this biological target and compounds tested against it in bioassay experiments.
Since HCV infection often persists in association with chronic hepatitis, it is appropriate to consider the natural history of HCV. We must determine what factors determine the clinical outcome of HCV infection and whether normalization of liver enzymes, with or without the presence of HCV RNA, is of any importance. The diagnosis and monitoring of HCV infection have become easier and more accurate with the quantitative and qualitative amplification techniques now available. However, the clinical relevance of the presence of HCV RNA, in correlation with serum ALT levels and HCV genotypes, is still not fully understood (18, 19).. Our study shows a very high concordance, 98.9%, between the bDNA assay and our single-step RT-PCR. Both assays target the same highly conserved region of HCV. The bDNA assay is highly reproducible and is unaffected by the genotypic variability of HCV (8); it is therefore a useful tool for monitoring HCV RNA levels throughout the course of disease. Our longitudinal ...
TY - JOUR. T1 - An interferon lambda 4-associated variant in the hepatitis C virus RNA polymerase affects viral replication in infected cells. AU - Bamford, Connor G.G.. AU - McLauchlan, John. PY - 2021/2/1. Y1 - 2021/2/1. N2 - Host IFNL4 haplotype status contributes to the development of chronic hepatitis C virus (HCV) infection in individuals who are acutely infected with the virus. In silico studies revealed that specific amino acid variants at multiple sites on the HCV polyprotein correlate with functional single-nucleotide polymorphisms (SNPs) in the IFNL4 locus. Thus, SNPs at the IFNL4 locus may select variants that influence virus replication and thereby the outcome of infection. Here, we examine the most significantly IFNL4-associated amino acid variants that lie in the lambda (L) 2 loop of the HCV NS5B RNA polymerase. L2 loop variants were introduced into both sub-genomic replicon and full-length infectious clones of HCV and viral replication was examined in the presence and absence ...
Recently, cell lifestyle systems producing hepatitis C virus particles (HCVcc) were developed. we developed serum-free culture systems producing high-titer single-density sf-HCVcc, showing similar biological properties as HCVcc. This methodology has the potential to advance HCV vaccine development and to facilitate biophysical studies of HCV. within the family. Due to a high degree of genetic heterogeneity, HCV has been categorized in 6 essential genotypes and several subtypes epidemiologically, differing in around 30% and 20% of their nucleotide and amino Vorinostat acidity sequence, [3 respectively,4]. Genotypes display important biological and clinical variations [5C10]. Serotypes Rabbit Polyclonal to 5-HT-2C. never have been defined; nevertheless, different genotypes and subtypes display differential level of sensitivity to neutralizing antibodies within sera of chronically contaminated patients also to monoclonal neutralizing antibodies with restorative potential [6,11C14]. The 9.6 kb HCV ...
TY - JOUR. T1 - Cutting edge. T2 - Identification of hepatitis C virus-specific CD8+ T cells restricted by donor HLA alleles following liver transplantation. AU - Rosen, Hugo R.. AU - Hinrichs, David J.. AU - Leistikow, Rachel L.. AU - Callender, Glenda. AU - Wertheimer, Anne M.. AU - Nishimura, Michael I.. AU - Lewinsohn, David M.. PY - 2004/11/1. Y1 - 2004/11/1. N2 - By necessity, human liver transplantation is performed across HLA barriers. As a result, intracellular infection of the allograft presents a unique immunologic challenge for the recipients immune system. In this study, we describe the presence of HLA-A2-restricted, hepatitis C virus (HCV)-specific CD8+ T cells in liver transplant recipients in whom the allograft is HLA-A2 positive and the recipient is HLA-A2 negative. These memory-effector T cells are recipient derived and recognize HCV peptide uniquely in the context of HLA-A2. Furthermore, these cells were absent before the transplant, suggesting that the allograft is capable ...
Hepatitis C virus subtype 3a is a highly prevalent and globally distributed strain that is often associated with infection via injection drug use. This subtype exhibits particular phenotypic characteristics. In spite of this, detailed genetic analysis of this subtype has rarely been performed. We performed full-length viral sequence analysis in 18 patients with chronic HCV subtype 3a infection and assessed genomic viral variability in comparison to other HCV subtypes. Two novel regions of intragenotypic hypervariability within the envelope protein E2, of HCV genotype 3a, were identified. We named these regions HVR495 and HVR575. They consisted of flanking conserved hydrophobic amino acids and central variable residues. A 5-amino-acid insertion found only in genotype 3a and a putative glycosylation site is contained within HVR575. Evolutionary analysis of E2 showed that positively selected sites within genotype 3a infection were largely restricted to HVR1, HVR495, and HVR575. Further analysis of ...
TY - JOUR. T1 - Dissecting the IFN-induced inhibition of hepatitis C virus replication by using a novel host cell line. AU - Windisch, Marc P.. AU - Frese, Michael. AU - Kaul, Artur. AU - Trippler, null. AU - Lohmann, Volker. AU - Bartenschlager, Ralf. PY - 2005. Y1 - 2005. N2 - The Hepatitis C virus (HCV), a member of the family Flaviviridae, is a major cause of chronic liver disease. Patients are currently treated with alpha interferon (IFN-alpha) that is given alone or in combination with ribavirin. Unfortunately, this treatment is ineffective in eliminating the virus in a large proportion of individuals. IFN-induced antiviral activities have been intensively studied in the HCV replicon system. It was found that both IFN-alpha and IFN-gamma inhibit HCV replicons, but the underlying mechanisms have not yet been identified. Of note is that nearly all of these studies were performed with the human hepatoma cell line Huh-7. Here, we report that genotypes 1b and 2a replicons also replicate in the ...
TY - JOUR. T1 - Gene expression profile of Li23, a new human hepatoma cell line that enables robust hepatitis C virus replication. T2 - Comparison with HuH-7 and other hepatic cell lines. AU - Mori, Kyoko. AU - Ikeda, Masanori. AU - Ariumi, Yasuo. AU - Kato, Nobuyuki. PY - 2010/12. Y1 - 2010/12. N2 - Human hepatoma cell line HuH-7-derived cells are currently the only cell culture system used for robust hepatitis C virus (HCV) replication. We recently found a new human hepatoma cell line, Li23, that enables robust HCV replication. Although both cell lines had similar liver-specific expression profiles, the overall profile of Li23 seemed to differ considerably from that of HuH-7. To understand this difference, the expression profile of Li23 cells was further characterized by a comparison with that of HuH-7 cells.Methods: cDNA microarray analysis using Li23 and HuH-7 cells was performed. Li23-derived ORL8c cells and HuH-7-derived RSc cells, in which HCV could infect and efficiently replicate, were ...
Persistent infection with hepatitis C virus (HCV) often causes chronic hepatitis, and then shows a high rate of progression to liver cirrhosis and hepatocellular carcinoma. To clarify the mechanism of the persistent HCV infection is considered to be important for the discovery of new target(s) for the development of anti-HCV strategies. In the present study, we found that the expression level of annexin A1 (ANXA1) in human hepatoma cell line Li23-derived D7 cells was remarkably lower than that in parental Li23 cells, whereas the susceptibility of D7 cells to HCV infection was much higher than that of Li23 cells. Therefore, we hypothesized that ANXA1 negatively regulates persistent HCV infection through the inhibition of viral RNA replication. The results revealed that HCV production was significantly inhibited without a concomitant reduction in the amount of lipid droplets in the D7 cells stably expressing exogenous ANXA1. Further, we demonstrated that ANXA1 negatively regulated the step of ...
Interferon alpha (IFN-α) is the key component of the therapy for hepatitis C virus (HCV) infection. IFN-α exerts anti-HCV activity by targeting certain signaling pathways. Using infectious HCV culture system in human hepatoma Huh7.5.1 cells, we analyzed functional relevance of extracellular signal-regulated kinase (ERK) pathway for IFN-α-mediated anti-HCV activity. IFN-α treatment resulted in activation of ERK pathway by increasing phosphorylation of c-Raf, MEK, and ERK1/2 in Huh7.5.1 cells, whereas HCV impaired such activation. IFN-α-dependent ERK1/2 phosphorylation was blocked by MEK inhibitor U0126. Pharmacological inhibition of ERK1/2 by U0126 or siRNA-mediated knockdown of ERK1/2 resulted in suppressive effects on HCV RNA levels and expression of HCV nonstructural protein 3 and envelope protein 2, establishing an important role for ERK pathway in HCV replication. Moreover, induction of a set of antiviral genes by IFN-α was enhanced in HCV-infected Huh7.5.1 cells due to the ERK1/2 knockdown,
AbstractChronic hepatitis C virus (HCV) infection is a major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma worldwide. With the recent development of direct acting antivirals (DAA), treatment of chronically infected patients has become highly effective although a subset of patients do not respond to therapy. Sofosbuvir is a common component of current de novo or salvage combination therapies. We used pre-treatment whole genome sequencing of HCV from 507 patients infected with HCV subtype 3a and treated with sofosbuvir containing regimens to detect viral polymorphisms associated with response to treatment. We found that three common polymorphisms present in HCV NS2 and NS3 proteins (not direct targets of sofosbuvir) were associated with reduced treatment response. These polymorphisms were enriched in post-treatment HCV sequences of patients unresponsive to treatment; they were also associated with lower reductions in viral load in the first week of therapy. The finding of
Genotypes of hepatitis C virus (HCV) present within 104 samples from HCV-infected individuals from Africa, the Middle East, the Indian subcontinent and South-East Asia were identified by sequence comparisons in the core and NS-5 regions. Relatively short sequences (such as the 222 bp fragment of NS-5) provided effective discrimination of types, subtypes and isolates, and produced equivalent relationships between genotypes as were found upon comparison of longer sequences of NS-5, of the core region, and by comparison of the limited number of complete genomic sequences currently available. Measurement of evolutionary distances in the core and NS-5 regions allowed 79 of the 104 samples to be identified as examples of known genotypes, while 17 of the remainder could be provisionally classified as new subtypes of types 1 (Nigeria), 2 (Gambia), 3 (India, Pakistan and Bangladesh) and 4 (Middle East) on the basis of sequence comparison in core and NS-5 (n = 9) or provisionally using core alone (n = 8). The
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Gentaur molecular products has all kinds of products like :search , AbD \ RECOMBINANT HEPATITIS C, Product Type Recombinant Protein, Specificity HEPATITIS C, Target Species Viral, Host N_A, Format Rec. Protein, Isotypes , Applications E, Clone \ 0100-0411 for more molecular products just contact us
Download Free Full-Text of an article THE DIFFERENCES IN GENE EXPRESSION PROFILE INDUCED BY GENOTYPE 1B HEPATITIS C VIRUS CORE ISOLATED FROM LIVER TUMOR AND ADJACENT NON-TU-MORAL TISSUE
By using the hepatitis C virus (HCV) genotype 2a JFH-1 or its chimeric strains, a HCV infection system has been previously developed through several methods- such as in vitro-transcribed JFH1-RNA transfection or stable transfection of the JFH1 cDNA into human hepatoma Huh-7 cell line or its derivatives. However, other reliable methods for delivery of the HCV genome into cells are still worth trying. The helper-dependent adenovirus (HDAd) is devoid of all viral coding sequences and has a package capacity of 37 kb, which is suitably large for the delivery of the HCV genome. Here we report a new method for delivery of the HCV genome into Huh-7 and HepG2 cells by using the HDAd vector. Our results demonstrated that the infection of Huh-7 cells with the HDAdJFH1 virus led to efficient HCV replication and virion production. We found that the HCV viral RNA levels could reach 107 copies per milliliter (ml) in the culture medium. HDAdJFH1-infected Huh-7 cells could be cultured for 8 passages with the culture
The present invention discloses nucleic acid sequences which encode infectious hepatitis C viruses and the use of these sequences, and polypeptides encoded by all or part of these sequences, in the development of vaccines and diagnostics for HCV and in the development of screening assays for the identification of antiviral agents for HCV.
Hepatitis C virus, illustration. Hepatitis C is most commonly spread by blood contact, through blood transfusions or the sharing of infected needles. It causes inflammation of the liver with jaundice and flu-like symptoms. There is currently no vaccine for hepatitis C. - Stock Image F019/2553
TY - JOUR. T1 - Intracellular proton conductance of the hepatitis C virus p7 protein and its contribution to infectious virus production. AU - Wozniak, Ann L.. AU - Griffin, Stephen. AU - Rowlands, David. AU - Harris, Mark. AU - Yi, Min Kyung. AU - Lemon, Stanley M.. AU - Weinman, Steven A.. PY - 2010/9/1. Y1 - 2010/9/1. N2 - The hepatitis C virus (HCV) p7 protein is critical for virus production and an attractive antiviral target. p7 is an ion channel when reconstituted in artificial lipid bilayers, but channel function has not been demonstrated in vivo and it is unknown whether p7 channel activity plays a critical role in virus production. To evaluate the contribution of p7 to organelle pH regulation and virus production, we incorporated a fluorescent pH sensor within native, intracellular vesicles in the presence or absence of p7 expression. p7 increased proton (H+) conductance in vesicles and was able to rapidly equilibrate H+ gradients. This conductance was blocked by the viroporin ...
DEB025 (Alisporivir) inhibits hepatitis C virus replication by preventing a cyclophilin A induced cis-trans isomerisation in domain II of ...
Goat polyclonal antibody raised against recombinant human hepatitis C virus. Recombinant protein corresponding to human hepatitis C virus. (PAB14675) - Products - Abnova
Here, we demonstrate querying of the HCVpro via the Hepatitis C Virus (HCV) proteins sub menu by browsing the list of HCV proteins. To retrieve interaction details on NS5A protein ...
A better understanding of natural variation in neutralization resistance and fitness of diverse hepatitis C virus (HCV) envelope (E1E2) variants will be critical to guide rational development of an HCV vaccine. This work has been hindered by inadequate genetic diversity in viral panels and by a lack of standardization of HCV entry assays. Neutralization assays generally use lentiviral pseudoparticles expressing HCV envelope proteins (HCVpp) or chimeric full-length viruses that are replication competent in cell culture (HCVcc). There have been few systematic comparisons of specific infectivities of E1E2-matched HCVcc and HCVpp, and to our knowledge, neutralization of E1E2-matched HCVpp and HCVcc has never been compared using a diverse panel of human broadly neutralizing monoclonal antibodies (bNAbs) targeting distinct epitopes. Here, we describe an efficient method for introduction of naturally occurring E1E2 genes into a full-length HCV genome, producing replication-competent chimeric HCVcc. We
Protease inhibitors (PIs) of hepatitis C virus (HCV) provide an additional or alternative therapy for chronic infection. However, assessment of their efficacy and ability to inhibit replication of different genotypes is hampered by the lack of a convenient animal model or a method for in vitro culture of HCV other than the type 1/2-based replicons and the infectious genotype 2a clone JFH1. To address this problem, we constructed a panel of replication-competent chimeric Jc1 (pFK JFH1/J6/C-846) clones containing protease and NS4A coding sequences from all six major genotypes, enabling the determination of replication and the susceptibility to PIs. Chimeras showed substantial variability in replication kinetics, attributable in part to naturally occurring polymorphisms and differing requirements for adaptive mutations in NS3 and NS4A. Through calculation of 50% inhibitory concentrations (IC(50)s) of BILN 2061, measuring reduction in the number of focus-forming units/ml (FFU/ml) and replication inhibition,
Hepatitis C virus (HCV) infection in humans is remarkably efficient in establishing viral persistence, leading to the development of liver cirrhosis and hepatocellular carcinoma. T cell responses have been reported to play a pivotal role in controlling HCV infection. However, HCV-specific T cell responses are significantly impaired in chronic HCV patients. This suggests that HCV may employ numerous mechanisms to counteract or possibly suppress the host T cell responses. Our laboratory is mainly focused on two inter-related arenas of biomedical research to elucidate the mechanism of HCV-mediated inhibition of T cell responses. Our research program involves both human and mouse studies. A better understanding of HCV-mediated immune regulation will provide a basis for the rational design of HCV therapeutics. Interaction of HCV-infected hepatocytes with NK cells and DC. The primary site of HCV replication occurs within hepatocytes in the liver. As a result of liver enodothelial cells perforated by ...
TY - JOUR. T1 - All-oral daclatasvir plus asunaprevir for hepatitis C virus genotype 1b. T2 - A multinational, phase 3, multicohort study. AU - Manns, Michael. AU - Pol, Stanislas. AU - Jacobson, Ira M.. AU - Marcellin, Patrick. AU - Gordon, Stuart C.. AU - Peng, Cheng Yuan. AU - Chang, Ting Tsung. AU - Everson, Gregory T.. AU - Heo, Jeong. AU - Gerken, Guido. AU - Yoffe, Boris. AU - Towner, William J.. AU - Bourliere, Marc. AU - Metivier, Sophie. AU - Chu, Chi Jen. AU - Sievert, William. AU - Bronowicki, Jean Pierre. AU - Thabut, Dominique. AU - Lee, Youn Jae. AU - Kao, Jia Horng. AU - McPhee, Fiona. AU - Kopit, Justin. AU - Mendez, Patricia. AU - Linaberry, Misti. AU - Hughes, Eric. AU - Noviello, Stephanie. N1 - Funding Information: This study was supported by Bristol-Myers Squibb. We thank Meghan Lovegren, Gail Denisky, and Mahnaz Mohebbian for their contributions to study execution. Editorial support was provided by Joy Loh, of Articulate Science, and was funded by Bristol-Myers Squibb. ...
Since its initial identification in St. Petersburg, Russia, the recombinant hepatitis C virus (HCV) 2k/1b has been isolated from several countries throughout Eurasia. The 2k/1b strain is the only recombinant HCV to have spread widely, raising questions about the epidemiological background in which it first appeared. In order to further understand the circumstances by which HCV recombinants might be formed and spread, we estimated the date of the recombination event that generated the 2k/1b strain using a Bayesian phylogenetic approach. Our study incorporates newly isolated 2k/1b strains from Amsterdam, The Netherlands, and has employed a hierarchical Bayesian framework to combine information from different genomic regions. We estimate that 2k/1b originated sometime between 1923 and 1956, substantially before the first detection of the strain in 1999. The timescale and the geographic spread of 2k/1b suggest that it originated in the former Soviet Union at about the time that the worlds first centralized
Hepatitis C Virus NS3山羊多克隆抗体(ab21124)经WB, ELISA, ICC/IF实验严格验证,被4篇文献引用。所有产品均提供质保服务,中国75%以上现货。
Merani, S., Petrovic, D., James, I., Chopra, A., Cooper, D., Freitas, E., Rauch, A., di Iulio, J., John, M., Lucas, M., Fitzmaurice, K., McKiernan, S., Norris, S., Kelleher, D., Klenerman, P. and Gaudieri, S. (2011), Effect of immune pressure on hepatitis C virus evolution: Insights from a single-source outbreak. Hepatology, 53: 396-405. doi: 10.1002/hep.24076 ...
All participants in the TURQUOISE-III trial, which enrolled HCV genotype 1b patients with compensated liver cirrhosis, achieved sustained virological response using AbbVies Viekira Pak or 3D regimen without ribavirin, according to a company announcement this week.. The advent of interferon-free direct-acting antiviral therapy has revolutionized hepatitis C treatment. But challenges remain for the most difficult-to-treat patients, including those with advanced liver disease.. TURQOUISE-III evaluated the 3D regimen in 60 cirrhotic patients with HCV genotype 1b. This is the most prevalent subtype in Europe and by far the most common in Japan, though harder-to-treat subtype 1a is more common in the U.S.. The 3D regimen consists of the HCV protease inhibitor paritaprevir with a ritonavir booster plus the NS5A inhibitor ombitasvir in a once-daily coformulation, taken with the NS5B polymerase inhibitor dasabuvir twice-daily. In the U.S. the full regimen is sold together under the brand name Viekira ...
Sigma-Aldrich offers abstracts and full-text articles by [Dorothee A Vogt, Grégory Camus, Eva Herker, Brian R Webster, Chia-Lin Tsou, Warner C Greene, Tien-Sze Benedict Yen, Melanie Ott].
Hepatitis C Virus NS5B protein antibody for WB. Anti-Hepatitis C Virus NS5B protein pAb (GTX131274) is tested in Hepatitis C virus samples. 100% Ab-Assurance.
The primary objective of this trial is to compare the efficacy of boceprevir (SCH 503034) 800 mg three times a day (TID) orally (PO) in combination with peginterferon alfa-2b (PegIFN-2b) 1.5 µg/kg weekly (QW) subcutaneously (SC) plus weight-based dosing (WBD) of ribavirin (RBV) (600 mg/day to 1400 mg/day) PO to therapy with PegIFN-2b + RBV alone in adult participants coinfected with human immunodeficiency virus (HIV) and previously untreated chronic hepatitis C virus (HCV) genotype 1.. Boceprevir is a potent, orally administered, novel serine protease inhibitor, specifically designed to inhibit the HCV nonstructural protein 3 (NS3) protease and, thereby, inhibit viral replication in HCV-infected host cells. The mechanism of inhibition represents a new mechanism of action compared to both interferon alfa and ribavirin. Based on previous experience with PegIFN-2b and RBV in combination with boceprevir in the HCV-monoinfected population, this combination treatment is expected to provide ...
The primary objective of this trial is to compare the efficacy of boceprevir (SCH 503034) 800 mg three times a day (TID) orally (PO) in combination with peginterferon alfa-2b (PegIFN-2b) 1.5 µg/kg weekly (QW) subcutaneously (SC) plus weight-based dosing (WBD) of ribavirin (RBV) (600 mg/day to 1400 mg/day) PO to therapy with PegIFN-2b + RBV alone in adult participants coinfected with human immunodeficiency virus (HIV) and previously untreated chronic hepatitis C virus (HCV) genotype 1.. Boceprevir is a potent, orally administered, novel serine protease inhibitor, specifically designed to inhibit the HCV nonstructural protein 3 (NS3) protease and, thereby, inhibit viral replication in HCV-infected host cells. The mechanism of inhibition represents a new mechanism of action compared to both interferon alfa and ribavirin. Based on previous experience with PegIFN-2b and RBV in combination with boceprevir in the HCV-monoinfected population, this combination treatment is expected to provide ...
Hepatitis C Virus NS4A protein antibody [497] for ELISA, WB. Anti-Hepatitis C Virus NS4A protein mAb (GTX19052) is tested in Hepatitis C virus samples. 100% Ab-Assurance.
BACKGROUND & AIMS: Tumor necrosis factor (TNF) is an inflammatory cytokine expressed by human fetal liver cells (HFLCs) after infection with cell culture-derived hepatitis C virus (HCV). TNF has been reported to increase entry of HCV pseudoparticles into hepatoma cells and inhibit signaling by interferon alpha (IFNα), but have no effect on HCV-RNA replication. We investigated the effects of TNF on HCV infection of and spread among Huh-7 hepatoma cells and primary HFLCs. METHODS: Human hepatoma (Huh-7 and Huh-7.5) and primary HFLCs were incubated with TNF and/or recombinant IFNA2A, IFNB, IFNL1, and IFNL2 before or during HCV infection. We used 2 fully infectious HCV chimeric viruses of genotype 2A in these studies: J6/JFH (clone 2) and Jc1(p7-nsGluc2A) (Jc1G), which encodes a secreted luciferase reporter. We measured HCV replication, entry, spread, production, and release in hepatoma cells and HFLCs. RESULTS: TNF inhibited completion of the HCV infectious cycle in hepatoma cells and HFLCs in a dose
Isolation and self-replication of infectious HCV has been a difficult task. However, this is needed for the purposes of developing rational drugs and for the analysis of the natural virus. Our recent report of an in vitro system for the isolation of human HCV from infected patients and their replication in tissue culture addresses this challenge. At California Institute of Molecular Medicine several isolates of HCV, called CIMM-HCV, were grown for over three years in cell culture. This is a report of the analysis of CIMM-HCV isolates for subtypes and quasispecies using a 269 bp segment of the 5UTR. HCV RNA from three patients and eleven CIMM-HCV were analyzed for this purpose. All isolates were essentially identical. Isolates of HCV from one patient were serially transmitted into fresh cells up to eight times and the progeny viruses from each transmission were compared to each other and also to the primary isolates from the patients serum. Some isolates were also transmitted to different cell types,
Hepatitis C virus (HCV) infection causes chronic liver diseases and is a global public health problem. Detailed analyses of HCV have been hampered by the lack of viral culture systems. Subgenomic replicons of the JFH1 genotype 2a strain cloned from an individual with fulminant hepatitis replicate ef …
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TY - JOUR. T1 - Hepatitis C virus RNA quantification in right and left lobes of the liver in patients with chronic hepatitis C. AU - Idrovo, V.. AU - Dailey, P. J.. AU - Jeffers, Lennox J. AU - Coelho-Little, E.. AU - Bernstein, D.. AU - Bartholomew, M.. AU - Alvarez, L.. AU - Urdea, M. S.. AU - Collins, M. L.. AU - Schiff, Eugene R. PY - 1996/9/1. Y1 - 1996/9/1. N2 - Quantification of hepatitis C virus RNA in liver tissue is likely to be useful in the study of the natural history, pathogenesis, progression and treatment of hepatitis C virus-associated liver disease. Quantitative measurements of hepatitis C virus RNA in liver biopsy samples using the branched DNA (bDNA) signal amplification assay were carried out. The aims of this study were threefold: first, to assess the level of hepatitis C virus RNA in biopsy samples from the right and left lobes of the liver; second, to evaluate the correlation between hepatitis C virus RNA levels in serum and liver; and third, to investigate the ...
BACKGROUND: CD4+ T cell help is critical in maintaining antiviral immune responses and such help has been shown to be sustained in acute resolving hepatitis C. In contrast, in evolving chronic hepatitis C CD4+ T cell helper responses appear to be absent or short-lived, using functional assays. METHODOLOGY/PRINCIPAL FINDINGS: Here we used a novel HLA-DR1 tetramer containing a highly targeted CD4+ T cell epitope from the hepatitis C virus non-structural protein 4 to track number and phenotype of hepatitis C virus specific CD4+ T cells in a cohort of seven HLA-DR1 positive patients with acute hepatitis C in comparison to patients with chronic or resolved hepatitis C. We observed peptide-specific T cells in all seven patients with acute hepatitis C regardless of outcome at frequencies up to 0.65% of CD4+ T cells. Among patients who transiently controlled virus replication we observed loss of function, and/or physical deletion of tetramer+ CD4+ T cells before viral recrudescence. In some patients with
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BACKGROUNDS & AIMS: The hepatitis C virus NS3 protein is taken up by myeloid cells in a TLR2-independent manner and activates myeloid cells via TLR2. This study aimed to identify the endocytic receptor(s) involved in the uptake of NS3 by myeloid cells and its relation with TLR2. METHODS: Inhibitors and transfected cells were used to identify the nature of the NS3-binding receptors expressed by myeloid cells. The cooperation between scavenger receptors (SRs) and TLR2 in the NS3-mediated activation of myeloid cells was evaluated using inhibitors, cells from TLR2(-/-) mice, and confocal microscopy. The involvement of SRs in NS3 cross-presentation was evaluated in vitro using an NS3-specific human T-cell clone. RESULTS: We observed that SRs are the main binding structures for NS3 on myeloid cells and identified the SRs SRA-1 and SREC-I as endocytic receptors for NS3. Moreover, both SRs and TLR2 cooperate in NS3-induced myeloid cell activation. CONCLUSION: This study highlights a central role for SRs in NS3
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The JFH1 replicon was less sensitive to CsA than were genotype 1b replicons.We compared the sensitivity of HCV replication to CsA in several subgenomic replicon cells. We used MH-14 (NN/1b/SG) and #50-1 (NN/1b/SG) cells carrying subgenomic replicons with HCV NN strain (15, 29), SN1 (Con1/1b/SG) cells carrying the Con1 subgenomic replicon (18), and sO (O/1b/SG) cells bearing the subgenomic O strain (12) as genotype 1b replicon-containing cells. We also employed JFH1#4-1 (JFH1/2a/SG) and JFH1#2-3 (JFH1/2a/SG) cell clones carrying the JFH1 subgenomic replicon (13). Treatment of CsA (1 μg/ml; 7 days) drastically decreased HCV RNA in all the subgenomic replicon cells carrying the HCV genotype 1b strain. HCV RNA levels in SN1 (Con1/1b/SG), MH-14 (NN/1b/SG), sO (O/1b/SG), and #50-1 (NN/1b/SG) cells decreased to 1/134, 1/219, 1/128, and 1/295, respectively (Fig. 3A). Genotype 1b replicon cells appeared highly sensitive to CsA. In contrast, the effect of CsA on HCV RNA levels in replicon cells ...
The recently developed subgenomic hepatitis C virus (HCV) replicons were limited by the fact the fact that series encoding the structural proteins was missing. contaminants, we pointed out that these cells discharge substantial levels of nuclease-resistant HCV RNA-containing buildings using a buoyant thickness of just one 1.04 to at least one 1.1 g/ml in iodixanol gradients. The same observation was manufactured in transient-replication assays using a geniune extremely modified full-length HCV genome that does not have heterologous sequences. Nevertheless, the actual fact that equivalent levels of such RNA-containing buildings were within the supernatant of cells holding subgenomic replicons demonstrates a non-specific discharge in addition to the presence from the structural protein. These results claim that Huh-7 cells lack host cell factors that are important for computer virus particle assembly and/or release. The hepatitis C computer virus (HCV) was identified as the causative agent for ...
Hepatitis C virus (HCV) infection causes significant morbidity and mortality among people who inject drugs (PWID) and HIV+ men who have sex with men (MSM). Characterizing spontaneous viral clearance of HCV infection among PWID and HIV+ MSM is important for assessing the burden of disease and treatment strategies in these populations. Electronic and other searches of medical literature were conducted. Reports were eligible if they presented original data from upper-middle- and high-income countries on laboratory-confirmed HCV infection and spontaneous viral clearance among PWID or HIV+ MSM. Pooled estimates of spontaneous viral clearance were generated using fixed-effect and random-effects models. Meta-regression examined potential predictors related to individual characteristics and research methodology. The meta-analysis estimated that spontaneous viral clearance occurs in 24.4 % of PWID and 15.4 % of HIV+ MSM. In univariate meta-regression among PWID, male sex and age were significantly associated
TY - JOUR. T1 - Daclatasvir for the treatment of chronic hepatitis C virus infection. AU - Temesgen, Zelalem. AU - Rizza, Stacey. PY - 2015/5/1. Y1 - 2015/5/1. N2 - Daclatasvir is a nonstructural protein 5A (NS5A) replication complex inhibitor that has shown potent in vitro activity against multiple hepatitis C virus (HCV) genotypes (GT). It is currently in advanced clinical development as a component of combination treatment regimens in a variety of HCV-infected patient populations. In studies conducted thus far, it has been generally well tolerated. It has been approved for the treatment of HCV GTs 1-4 in the European Union. The combination of daclatasvir and asunaprevir (an HCV NS3/4A protease inhibitor) has been approved in Japan for the treatment of patients with GT1 HCV infection. Here we review the available literature on daclatasvir, including its information on its discovery, mechanism of action, pharmacology, preclinical and clinical activity, resistance and safety.. AB - Daclatasvir ...
Hepatitis C is a common cause of chronic liver disease but is rarely associated with acute hepatitis. The majority of patients have no clinical symptoms and jaundice in this phase of acute viral hepatitis C. Clinical symptoms are not difference with other types of hepatitis [2]. It is necesseray to treat acute hepatitis C infection. HCV infection becomes chronic in about 85 % of individuals as demonstrated by the persistence of HCV. HCV is the major cause of cirrhosis and hepatocellular carcinoma [2]. Interferon-α is effective in improving biochemical outcomes and achieving sustained virologic clearance in patients with acute hepatitis C [3]. If acute infection is confirmed (with or without acute hepatitis), recent data suggest that early treatment of acute HCV infection with interferon-α may be highly effective in preventing chronic HCV infection [1]. These data underscore the importance of identifying persons with acute HCV infection and promptly referring them to experienced clinicians who ...
TY - JOUR. T1 - Determinants of viral clearance and persistence during acute hepatitis C virus infection. AU - Thimme, Robert. AU - Oldach, David. AU - Chang, Kyong Mi. AU - Steiger, Carola. AU - Ray, Stuart C.. AU - Chisari, Francis V.. PY - 2001/11/19. Y1 - 2001/11/19. N2 - The virological and immunological features of hepatitis C virus (HCV) infection were studied weekly for 6 months after accidental needlestick exposure in five health care workers, four of whom developed acute hepatitis that progressed to chronicity while one subject cleared the virus. In all subjects, viremia was first detectable within 1-2 weeks of inoculation, 1 month or more before the appearance of virus-specific T cells. The subject who cleared the virus experienced a prolonged episode of acute hepatitis that coincided with a CD38+ IFN-γ- CD8+ T cell response to HCV and a small reduction in viremia. Subsequently, a strong CD4+ T cell response emerged and the CD8+ T cells became CD38- and started producing IFN-γ in ...
Hepatitis C virus (HCV) infection leads to severe liver diseases including hepatocellular carcinoma (HCC). Phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a tumour suppressor, is frequently mutated or deleted in HCC tumors. PTEN has previously been demonstrated to inhibit HCV secretion. In this study, we determined the effects of PTEN on the other steps in HCV life cycle, including entry, translation, and replication. We showed that PTEN inhibits HCV entry through its lipid phosphatase activity. PTEN has no effect on HCV RNA translation. PTEN decreases HCV replication and the protein phosphatase activity of PTEN is essential for this function. PTEN interacts with the HCV core protein and requires R50 in domain I of HCV core and PTEN residues 1-185 for this interaction. This interaction is required for PTEN-mediated inhibition of HCV replication. This gives rise to a reduction in PTEN levels and intracellular lipid abundance, which may in turn regulate HCV replication. HCV core domain I
Interaction between hepatitis C virus core protein and translin protein- a possible molecular mechanism for hepatocellular carcinoma and lymphoma caused by hepatitis C virus
333076442 - EP 2305695 A2 2011-04-06 - Macrocyclic inhibitors of Hepatitis C virus replication - The embodiments provide compounds of the general Formulae I through general Formula VIII, as well as compositions, including pharmaceutical compositions, comprising a subject compound. The embodiments further provide treatment methods, including methods of treating a hepatitis C virus infection and methods of treating liver fibrosis, the methods generally involving administering to an individual in need thereof an effective amount of a subject compound or composition.[origin: WO2007015824A2] The embodiments provide compounds of the general Formulae (I) through general Formula (VIII), as well as compositions, including pharmaceutical compositions, comprising a subject compound. The embodiments further provide treatment methods, including methods of treating a hepatitis C virus infection and methods of treating liver fibrosis, the methods generally involving administering to an individual in need thereof an
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Treatment of chronic hepatitis C virus (HCV) infection with interferon (IFN) and ribavirin improves the rate of eradication of HCV, but only about 13-14% of non-responders (NR) with HCV of genotype 1b previously treated with IFN achieve a sustained virological response (SVR). To determine whether HCV quasispecies diversity correlates with the outcome of therapy with IFN and ribavirin, we studied 13 patients undergoing combination therapy with IFN-alpha2b and ribavirin after failure of IFN monotherapy. HCV quasispecies diversity was assessed by cloning and sequencing before and during combination therapy. During therapy, quasispecies diversity diminished in NR patients, both in the hypervariable region (HVR) 1 of the envelope 2 (E2) domain and in the interferon sensitivity-determining region (ISDR) in the NS5A. Pre-treatment nucleotide quasispecies diversity was lower in SVR and end-of-therapy viral response (ETR) patients than in NR patients. Resistance to ribavirin was associated with high pre
Product Name: Mouse mAb anti- human hepatitis C virus (HCV) non-structural protein NS-4, Clone 101Collection: AntibodySub Category: Monoclonal
A major concern across the globe and especially in the developing countries is increasing burden of infectious diseases on healthcare system. Burden of hepatitis C virus infection is growing over the years. Approximately 3% of global population is infected with hepatitis C virus infection, according to Institute of Liver and Biliary Sciences, India. HCV leads to chronic infection in 80% of infected patients. Initial testing for hepatitis C virus uses serological assays to detect antibodies against HCV in blood samples.. Europe is expected to dominate the Hepatitis C Virus Testing Market significantly due to increasing prevalence of hepatitis C virus diseases. According to WHO, Europe has 1.5% prevalence of HCV diseases due to high rates of mutation of viral RNA that shows significant variations in genes in population globally.. Asia Pacific is expected to be having lucrative market growth over the forecast period owing to disease prevalence rates in the developing and underdeveloped countries. ...
A major concern across the globe and especially in the developing countries is increasing burden of infectious diseases on healthcare system. Burden of hepatitis C virus infection is growing over the years. Approximately 3% of global population is infected with hepatitis C virus infection, according to Institute of Liver and Biliary Sciences, India. HCV leads to chronic infection in 80% of infected patients. Initial testing for hepatitis C virus uses serological assays to detect antibodies against HCV in blood samples.. Europe is expected to dominate the Hepatitis C Virus Testing Market significantly due to increasing prevalence of hepatitis C virus diseases. According to WHO, Europe has 1.5% prevalence of HCV diseases due to high rates of mutation of viral RNA that shows significant variations in genes in population globally.. Asia Pacific is expected to be having lucrative market growth over the forecast period owing to disease prevalence rates in the developing and underdeveloped countries. ...
Hepatitis C virus RNA replication requires not only the viral replicase but also the host cytoskeletons, membrane structures, and cellular factors. Several hnRNPs, such as polypyrimidin-tract-binding protein (PTB) and La autoantigen were found to regulate both HCV RNA replication and translation. Another hnRNP, SYNCRIP (synaptotamin-Binding, Cytoplasmic RNA-Interacting Protein, or NSAP-1), was found to regulate HCV-IRES dependent translation. In my first part of dissertation, we identified SYNCRIP as a positive regulator of HCV RNA replication.; With a growing number of dual-function proteins which are able to regulate HCV RNA translation and replication, it is interesting to investigate how the two important steps in HCV life cycle are temporally and spatially regulated. Therefore, we initiated a series of experiments to examine if HCV RNA translation is dependent on its replication. The colocalization of newly-synthesized viral RNA and peptide were detected in live cell and under ...
There is no currently approved treatment for acute HCV infection. Guidelines recommend 24 weeks of therapy with interferon (IFN) and ribavirin in HIV coinfected individuals who are diagnosed with acute HCV. Shorter duration therapy with all-oral agents may offer a better-tolerated more efficacious alternative. Here we evaluated the safety, tolerability and efficacy of ledipasvir (LDV)/sofosbuvir (SOF) fixed dose combination for 6 weeks in genotype 1 or 4 HIV-infected patients with acute HCV infection.. Patients with an acute HCV infection of ,24 weeks duration as per NEAT AHC guidelines were included. Patients were required to either be receiving HIV antiretroviral (ARV) therapy with HIV RNA ,200 copies/mL, or not be receiving any treatment for HIV with no plans to start therapy. Enrollment of patients with active illicit drug use was permitted. Patients with acute opportunistic infections or HBV co-infection were excluded. The primary endpoint was sustained viral response defined as HCV ...
Importance. Hepatitis C virus (HCV) is the most common chronic blood-borne pathogen in the US and a leading cause of complications from chronic liver disease.1 Hepatitis C virus infection is associated with more deaths than the top 60 other reportable infectious diseases combined, including HIV.2 The most important risk factor for HCV infection is past or current injection drug use.1 In the US, an estimated 4.1 million persons have past or current HCV infection (ie, they test positive for the anti-HCV antibody). Of these persons who test positive for the anti-HCV antibody, approximately 2.4 million have current infections based on testing with molecular assays for HCV RNA.1, 3-5 The estimated prevalence of chronic HCV infection is approximately 1.0% (2013 to 2016).6 An estimated 44,700 new HCV infections occurred in the US in 2017.7 Cases of acute HCV infection have increased approximately 3.8-fold (2010 to 2017) over the last decade because of increasing injection drug use and improved ...
Line immunoassay for the detection of antibodies to human hepatitis C virus in human serum and plasma. It is intended for use as a supplementary test on human serum or plasma specimens found to be reactive in an anti-HCV screening procedure.
article{DaneshEtalHCV, author = {Danesh, Gonché and Virlogeux, Victor and Ramière, Christophe and Charre, Caroline and Cotte, Laurent and Alizon, S}, title = {{Quantifying transmission dynamics of acute hepatitis C virus infections in a heterogeneous population using sequence data}}, journal={\emph{PCI Evol Biol}}, volume={689158, ver. 5}, year={2021}, doi = {10.24072/pci.evolbiol.100117}, Bdsk-url-1 = {https://evolbiol.peercommunityin.org/articles/rec?id=217&reviews=True}, URL= {https://www.biorxiv.org/content/10.1101/689158v6.full.pdf ...
Underascertainment of acute hepatitis C virus infections in the U.S. surveillance system: a case series and chart review. Ann Intern Med. 2015 Aug 18; 163(4):254-61 ...
We read with interest the paper by Himmelsbach and colleagues discussing the role of sorafenib in blocking hepatitis C virus (HCV) replication in vitro.1 Further studies are required to delineate the potential antiviral efficacy either in combination with the standard of care (Peg-IFN and ribavirin) or as monotherapy. Currently, a number of new antiviral drugs are being investigated in order to improve sustained virological response (SVR) rates and/or reduce treatment duration in chronic hepatitis C (CHC). However, to date none of the new small molecule drugs appear effective against genotype 3 such that at the present time patients with genotype 3 infection have no other options.. Debio 025 is a selective cyclophilin inhibitor that has previously demonstrated antiviral activity against the hepatitis C virus both in vitro and in vivo.2 3 Results of a phase Ib study indicate that Debio 025 has an important additive anti-HCV effect when coadministered with Peg-interferon (IFN)α-2a to ...
TY - JOUR. T1 - Vaccination against hepatitis C virus infection. T2 - Miles to go before we sleep. Choo Q-L, Kuo G, Ralston R, Weiner A, Chien D, Van Nest G, Han J, Berger K, Thudium K, Kuo C, Kansopon J, McFarland J, Tabrizi A, Ching K, Moss B, Cummins LB, Houghton M, Muchmore E. Vaccination of chimpanzees against infection by the hepatitis C virus. Proc Natl Acad Sci U S A 1994;91:1294-1298. AU - Koziel, Margaret James. AU - Liang, T. Jake. PY - 1994/9. Y1 - 1994/9. N2 - A high incidence of community-acquired hepatitis C virus infection that can lead to the progressive development of chronic active hepatitis, liver cirrhosis, and primary hepatocellular carcinoma occurs throughout the world. A vaccine to control the speread of this agent that represents a major cause of chronic liver disease is therefore needed. Seven chimpanzees (Pan troglodytes) have been immunized with both putative envelope glycoproteins [E1 (pg33) and E2 (pg72)] that were copurified from HeLa cells infected with a ...
Author Summary One of the key components for hepatitis C virus (HCV) propagation is lipids, some of which comprise membranous replication complexes for HCV replication. Research on cofactors that are involved in the formation of the membranous replication complex has advanced steadily; on the other hand, the lipids constituting the membranous replication complex remain to be elucidated. Here, we report that HCV modulates sphingolipid metabolism by promoting sphingolipid biosynthesis, to enhance viral replication. Specifically a specific molecular species of sphingomyelin (SM), a type of sphingolipid interacts with HCV nonstructural 5B polymerase, enhancing HCV replication. This work highlights the relationship between specific molecular species of SMs and HCV replication, giving new insight into the formation of the HCV replication complex and the involvement of host lipids in the HCV life cycle.
Mouse anti Hepatitis C NS-3 Antigen antibody, clone BGN/1244/3B5 recognizes the Hepatitis C virus non-structural protein 3 (NS3).
Subgenomic replicons of hepatitis C virus (HCV) have been widely used for studying HCV replication. Here, we report a new subgenomic replicon based on a strain isolated from a chronically infected pat
This Application Note shows how the Dual luciferase assay can help to assess the Replication of the Hepatitis C Virus subgenomic replicon. Read more.
Title: Emerging Therapeutic Strategies for Hepatitis C Virus Infection. VOLUME: 1 ISSUE: 2. Author(s):Ken Sato, Hitoshi Takagi, Takeshi Ichikawa, Satoru Kakizaki and Masatomo Mori. Affiliation:Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, 3-39-15 Showa, Maebashi, Gunma 371-8511, Japan.. Keywords:Hepatitis C virus, therapy, target, inhibitor, effectiveness, safety, resistance, clinical studies. Abstract: The universal prevalence of hepatitis C virus (HCV) infection, which causes chronic hepatitis, cirrhosis, liver failure, and hepatocellular carcinoma, has become a significant health problem worldwide. Interferon-based therapies, the current standard, IFN-based therapies have limited efficacy and undesirable adverse effects. In addition, neither vaccination against HCV nor specific antiviral reagents for HCV are yet available. Thus, a major medical need still exists for novel and more efficacious anti-HCV reagents showing broad-spectrum clinical ...
TY - JOUR. T1 - Persistently normal aminotransferase in chronic hepatitis C virus infection. T2 - Is it time to redefine parameters of normality?. AU - Giannini, E.. AU - Testa, R.. PY - 2001. Y1 - 2001. UR - http://www.scopus.com/inward/record.url?scp=0035071120&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0035071120&partnerID=8YFLogxK. M3 - Article. C2 - 11346151. AN - SCOPUS:0035071120. VL - 33. SP - 202. EP - 203. JO - Digestive and Liver Disease. JF - Digestive and Liver Disease. SN - 1590-8658. IS - 2. ER - ...
Innate CD56(pos) natural killer (NK) and natural T (NT) cells comprise important hepatic antiviral effector lymphocytes whose activity is fine-tuned through surface NK receptors (NKRs). Dysregulation of NKRs in patients with long-standing hepatitis C virus (HCV) infection has been shown, but little is known regarding NKRs in acute infection. Treatment-naïve patients with acute HCV (n = 22), including 10 with spontaneous recovery, were prospectively studied. CD56(pos) NT levels were reduced early in acute HCV infection and did not fluctuate over time. In resolving HCV infection, NT cells with a more activated phenotype (lower CD158A and higher natural cytotoxicity receptor expression) at baseline predated spontaneous recovery. Moreover, NKG2A expression on CD56(+) NT cells correlated directly with circulating HCV RNA levels. Deficient interleukin-13 (IL-13) production by NT cells and reduced IL-2-activated killing (LAK) at baseline were associated with the ultimate development of persistence. ...
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79036 avhandlingar från svenska högskolor och universitet. Avhandling: Development of vaccines and mouse models for chronic hepatitis C virus infection.
TY - JOUR. T1 - The importance of rapid viral suppression in the era of directly acting antiviral therapy for hepatitis C virus.. AU - Jenkins, Erin T.. AU - Jensen, Donald M.. PY - 2012/12. Y1 - 2012/12. N2 - An increased understanding of viral kinetics has allowed clinicians to tailor therapy for hepatitis C virus through identifying patients who have the best chance of viral eradication and those for whom therapy will likely fail. Nonetheless, sustained viral response rates with pegylated interferon (PegIFN) and ribavirin remain disappointingly low. However, exciting advancements in the field of hepatitis C therapy include the development of new direct-acting antiviral agents, which offer much higher rates of sustained viral eradication when used in combination with PegIFN and ribavirin.. AB - An increased understanding of viral kinetics has allowed clinicians to tailor therapy for hepatitis C virus through identifying patients who have the best chance of viral eradication and those for whom ...
Cellular immune responses are likely to play a key role in determining the clinical outcome in acute infection with hepatitis C virus (HCV), but the dynamics of such responses and their relationship to viral clearance are poorly understood. In a previous study we have shown highly activated, multispecific cytotoxic T lymphocyte responses arising early and persisting in an individual who subsequently cleared the virus. In this study the HCV-specific CD8+ lymphocytes response has been similarly analyzed, using peptide-HLA class I tetramers, in a further nine individuals with documented acute HCV infection, six of whom failed to clear the virus. Significant populations of virus-specific CD8+ lymphocytes were detected at the peak of acute hepatic illness (maximally 3.5% of CD8+ lymphocytes). Frequencies were commonly lower than those seen previously and were generally not sustained. Early HCV-specific CD8+ lymphocytes showed an activated phenotype in all patients (CD38+ and HLA class II+), but this
Hepatitis C virus (HCV) infection is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. It is estimated that 1% of the general population in Western Europe and North America and 380 million people globally are infected with HCV worldwide (19). A protective vaccine does not exist to date, and therapeutic options are still limited. HCV has been classified in the Hepacivirus genus within the Flaviviridae family of viruses. It contains a 9.6-kb plus-strand RNA genome (10, 59, 70) composed of a 5′ noncoding region (5′ NCR), a long open reading frame (ORF) encoding a polyprotein precursor of about 3,000 amino acids (aa), and a 3′ NCR. The HCV polyprotein precursor is co- and posttranslationally processed by cellular and viral proteases to yield the mature structural and nonstructural (NS) proteins. The structural proteins include the core protein, which forms the viral nucleocapsid, and the envelope glycoproteins E1 and E2. They are separated from the NS proteins ...
Hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is a remarkable protein as it clearly plays multiple roles in mediating viral replication, host-cell interactions and viral pathogenesis. However, on the impact of cell growth, there have been different study results. NS5ATP9, also known as KIAA0101, p15PAF, L5, and OEACT-1, was first identified as a proliferating cell nuclear antigen-binding protein. Earlier studies have shown that NS5ATP9 might play an important role in HCV infection. The aim of this study is to investigate the function of NS5ATP9 on hepatocellular carcinoma (HCC) cell lines proliferation under HCV NS5A expression. The results showed that overexpression of NS5ATP9 inhibited the proliferation of Bel7402 cells, whereas knockdown of NS5ATP9 by interfering RNA promoted the growth of HepG2 cells. Under HCV NS5A expression, RNA interference (RNAi) targeting of NS5ATP9 could reverse the inhibition of HepG2 cell proliferation, suggesting that NS5ATP9 might be an anti-proliferation gene
Hepatitis C virus (HCV) genotyping is a tool used to optimize antiviral treatment regimens. The newly developed Versant HCV genotype assay (LiPA) 2.0 uses sequence information from both the 5 untranslated region and the core region, allowing distinction between HCV genotype 1 and subtypes c to l of genotype 6 and between subtypes a and b of genotype 1. HCV-positive samples were genotyped manually using the Versant HCV genotype assay (LiPA) 2.0 system according to the manufacturers instructions. For the comparison study, Versant HCV genotype assay (LiPA) 1.0 was used. In this study, 99.7% of the samples could be amplified, the genotype of 96.0% of samples could be determined, and the agreement with the reference method was 99.4% when a genotype was determined. The reproducibility study showed no significant differences in performance across sites (P = 0.43) or across lots (P = 0.88). In the comparison study, 13 samples that were uninterpretable or incorrectly genotyped with Versant HCV genotype ...
This study was conducted to examine, in vitro , the effect of soluble egg antigen (SEA) of S. haematobium on intracellular HCV RNA load in peripheral mononuclear cells (PBMC) as well as on cell proliferation in patients with chronic HCV infection. PBMC from 26 patients with chronic HCV infection were cultured for 72 hours in presence and absence of 50 μg SEA/ml medium. Intracellular HCV RNA quantification of plus and minus strands was assessed before and after stimulation. PBMC from five healthy subjects were cultured for 7 days, flow cytometric analysis of DNA content was used to assess the mitogenic effect of SEA on PBMC proliferation compared to phytoheamaglutinine (PHA). Quantification of the intracellular viral load showed increased copy number/cell of both or either viral strands after induction with SEA in 18 of 26 patients (69.2%) thus indicating stimulation of viral replication. Flow cytometric analysis showed that mean ± S.D. of percent values of cell proliferation was induced from 3.2 ± 1