Clearance of HCV RNA following acute hepatitis A superinfection
Department of Internal Medicine and Medical Specialties, Via Passo Gravina 187, I-95127 Catania, Italy. Digestive and Liver Disease
(Impact Factor: 2.96).
02/2008; 41(5):371-4. DOI: 10.1016/j.dld.2007.11.015
A transient reduction of hepatitis C virus replication during the course of acute hepatitis A virus infection has already been reported in the literature. The present study reports the case study of a subject with chronic hepatitis due to hepatitis C virus who went on to develop an acute hepatitis A. From the early onset of acute disease, hepatitis C virus ribonucleic acid became undetectable. Following recovery from acute hepatitis, alanine amino-transferase levels became persistently normal and liver biopsy revealed a reduction in the Knodell histological activity index score. Hepatitis C virus ribonucleic acid clearance was maintained up to 4 years after the onset of acute hepatitis A. During the course of the acute disease, a sharp increase in interferon gamma levels was detected in serum and in the supernatant of both unstimulated and phytoemagglutinin/lipopolysaccharide-stimulated peripheral blood mononuclear cells. Interferon gamma levels were still high 3 months later. We hypothesize that acute hepatitis A virus superinfection during the course of chronic hepatitis C may lead to hepatitis C virus ribonucleic acid clearance through an immunological mechanism related to interferon gamma production.
Available from: Seung-Woon Paik
- "However, because a reduction in HBV viral load is associated with an increase in the immune response of the host, in some cases an excessive host response may induce severe damage of hepatocytes. Although their study was not on hepatitis B, Cacopardo et al.14 suggested that HAV and HCV-related liver cell damage and viral clearance might be mediated by HAV-specific T cell responses with enhanced production of INF-γ. Several studies have reported that HAV superinfection in patients with pre-existing liver disease is associated with a high rate of morbidity and mortality.15-19 "
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ABSTRACT: The notion that acute hepatitis A superimposed on chronic hepatitis B infection leads to a worse outcome than acute hepatitis A alone remains controversial. The aim of this study was to determine the influence of the presence of hepatitis B surface antigen (HBsAg) on the severity of acute hepatitis A.
We retrospectively analyzed 449 patients hospitalized for acute hepatitis A from January 2000 to February 2010 and compared clinical outcomes based on the presence of HBsAg.
Of the 449 patients, 30 patients were in the HBsAg-positive group and 419 in the HBsAg-negative group. The HBsAg-positive group was older than the HBsAg-negative group (36.1±8.3 vs 31.8±8.5 years, p=0.004); however, other baseline characteristics were similar between the 2 groups. Mean peak values of prothrombin time, serum total bilirubin, and serum creatinine at admission were significantly higher in the HBsAg-positive group. When comparing clinical outcomes between the 2 groups, gastrointestinal bleeding, acute renal failure, and acute liver failure were more frequently observed in the HBsAg-positive group. In particular, the incidence of acute liver failure was approximately 9-fold higher in the HBsAg-positive group than in the HBsAg-negative group (23.3% vs 3.3%; odds ratio [OR], 8.80; p<0.001). Multivariate analysis showed that HBsAg (OR, 7.43; 95% confidence interval [CI], 2.56 to 21.57) and age (OR, 1.07; 95% CI, 1.02 to 1.13) were independent risk factors for the occurrence of acute liver failure.
In patients with chronic hepatitis B infection, acute hepatitis A is associated with more severe clinical outcomes, including acute liver failure, compared with patients with acute hepatitis A alone.
Gut and liver 12/2011; 5(4):500-5. DOI:10.5009/gnl.2011.5.4.500 · 1.81 Impact Factor
Available from: Daniel Schulte
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ABSTRACT: Recent experimental results on normal conducting RF structures indicate that the scaling of the gradient limit with frequency is less favourable than was believed. We therefore reconsider the optimum choice of RF frequency and iris aperture for a normal conducting, two-beam linear collider with E<sub>CMS</sub>=3 TeV, a loaded accelerating gradient of 150 MV/m and a luminosity of 8·10<sup>34</sup>cm<sup>-2</sup>s<sup>-1</sup>. The optimisation criterion is minimizing RF costs for investment and operation with constraints put on peak surface electric fields and pulsed heating of accelerating structures. Analytical models are employed where applicable, while interpolation of simulation program results is used for the calculation of luminosity and RF structure properties.
Particle Accelerator Conference, 2003. PAC 2003. Proceedings of the; 06/2003
Available from: Matthias Ocker
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ABSTRACT: The anti-inflammatory and antiapoptotic heme degrading enzyme heme oxygenase-1 (HO-1) has been shown recently to interfere with replication of hepatitis C virus (HCV). We investigated the effect of HO-1 products carbon monoxide (CO), iron and biliverdin on HCV replication using the replicon cell lines Huh-5-15 and LucUbiNeo-ET, stably expressing HCV proteins NS3 through NS5B. Incubation of these cell lines in the presence of the CO donor methylene chloride transiently reduced HCV replication, whereas an increase of iron in cell culture by administration of FeCl(3) or iron-saturated lactoferrin did not interfere with HCV replication. Likewise, depletion of iron by deferoxamine during induction of HO-1 by cobalt-protoporphyrin IX did not restore HCV replication. The most prominent effect was observed after incubation of replicon cell lines in the presence of biliverdin. Biliverdin seems to interfere with HCV replication-mediated oxidative stress by inducing expression of antiviral interferons, such as interferon alpha2 and alpha17. CONCLUSION: The antioxidant biliverdin reduces HCV replication in vitro by triggering the antiviral interferon response and might improve HCV therapy in the future.
Hepatology 02/2010; 51(2):398-404. DOI:10.1002/hep.23339 · 11.06 Impact Factor
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