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Hepatitis B Viruses (hepatitis + b_viruse)
Selected AbstractsPathogen-reduction methods: advantages and limitsISBT SCIENCE SERIES: THE INTERNATIONAL JOURNAL OF INTRACELLULAR TRANSPORT, Issue 1 2009H. G. Klein Pathogen-reduction (inactivation) provides a proactive approach to reducing transfusion-transmitted infection. Pathogen-reduction technologies have been successfully implemented by plasma fractionators resulting in no transmission of human immunodeficiency, hepatitis C, or hepatitis B viruses by US-licensed plasma derivatives since 1987. Fractionation technologies cannot be used to treat cellular blood components. Although blood donor screening, deferral and disease testing have drastically reduced the incidence of transfusion-transmitted diseases, the threat of new or re-emerging pathogens remains. Of particular concern is the silent emergence of a new agent with a prolonged latent period in which asymptomatic infected carriers would donate and spread infection. The ultimate goal of pathogen-inactivation is to reduce transmission of potential pathogens without significantly compromising the therapeutic efficacy of the cellular and protein constituents of blood. The acceptable technology must not introduce toxicities into the blood supply nor result in neoantigen formation and subsequent antibody production. Several promising pathogen-inactivation technologies are being developed and tested, and others are currently in use, but all of them have limits. Pathogen-reduction promises an additional ,layer of protection' from infectious agents and has the potential to impact the safety of blood transfusions worldwide. [source] Molecular, immunological and clinical properties of mutated hepatitis B virusesJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 1 2002C. Kreutz Abstract Hepatitis B virus (HBV) is at the origin of severe liver diseases like chronic active hepatitis, liver cirrhosis and hepatocellular carcinoma. There are some groups of patients with high risk of generation of HBV mutants: infected infants, immunosupressed individuals (including hemodialysis patients), patients treated with interferon and lamivudine for chronic HBV infection. These groups are the target for molecular investigations reviewed in this paper. The emergence of lamivudine- or other antiviral-resistant variants, rises concern regarding long term use of these drugs. Infection or immunization with one HBV subtype confers immunity to all subtypes. However, reinfection or reactivation of latent HBV infection with HBV mutants have been reported in patients undergoing transplant and those infected with HIV. Mutations of the viral genome which are not replicative incompetent can be selected in further course of infection or under prolonged antiviral treatment and might maintain the liver disease. Four open reading frames (ORF) which are called S-gene, C-gene, X-gene and P-gene were identified within the HBV genome. Mutations may affect each of the ORFs. Mutated S-genes were described to be responsible for HBV-infections in successfully vaccinated persons, mutated C-genes were found to provoke severe chronic liver diseases, mutated X-genes could cause serious medical problemes in blood donors by escaping the conventional test systems and mutated P-genes were considered to be the reason for chemotherapeutic drug resistance. This paper reviews molecular, immunological and clinical aspects of the HBV mutants. [source] Prediction of response to treatment of chronic hepatitis B with pegylated interferon in the PhilippinesJOURNAL OF MEDICAL VIROLOGY, Issue 2 2010Dorothy M. Agdamag Abstract The response marker for interferon has not been investigated fully for hepatitis B viruses (HBVs) in the Philippines where novel subtypes B5 and C5 were recognized recently. The prediction parameters for interferon treatment were assessed, with emphasis on the mutation patterns in the basal core promoter and precore regions in patients with chronic hepatitis B. Seventeen HBeAg-positive patients were stratified according to response to treatment with pegylated interferon based on HBe seroconversion and HBV load. Intra-patient distributions of wild-type strains (A1762, G1764) and variants (T1762, A1764) were analyzed using HBV-DNA amplification and subsequent molecular cloning. The rate of variants (T1762, A1764) harbored by a patient was higher among responders (41.2% and 31% per person on average) than among non-responders (2.4% and 2.4%) to treatment with pegylated interferon at the baseline, respectively (P,<,0.05). The rate of variants (T1762, A1764) harbored by responders (41.2% and 31%) decreased to 1.7% and 1.7%, and wild-type strains (A1762, G1764) conversely became majority (98.3% and 98.3%) after treatment with pegylated interferon, respectively. HBV strains harbored by two of six responders and a patient with lower baseline load (1.0,×,104,copies/ml) showed genotype shift from A to other genotypes, where genotype A disappeared preferentially after the loss of HBeAg and genotypes B and C formed a major population. These results suggest that the HBV variants (T1762, A1764) and HBV genotype A in the Philippines have an advantage in the response to pegylated interferon. These results warrant a large-scale examination for further precise prediction of the response to treatment with interferon. J. Med. Virol. 82:213,219, 2010. © 2009 Wiley-Liss, Inc. [source] Sequencing of human-viral DNA junctions in hepatocellular carcinoma from patients with HCV and occult HBV infectionJOURNAL OF MEDICAL VIROLOGY, Issue 4 2003Akihiro Tamori Abstract DNA of free hepatitis B viruses (HBV) has been detected in the liver of patients infected with hepatitis C virus (HCV). It is unknown whether HBV DNA is integrated into such livers; if so, it may affect hepatocarcinogenesis. Hepatocellular carcinomas (HCCs) from 34 patients without HBV surface antigen (HBsAg) and with anti-HCV, and from 7 patients with HBsAg and without anti-HCV as controls, were examined, using the cassette-ligation,mediated polymerase chain reaction and primers based on HBV DNA sequence. In the controls, HBV DNA had been integrated into human DNA of all HCCs. On the basis of HBV DNA in tumor tissue, 23 of the 34 patients with anti-HCV had occult infection. Junctions between human DNA and HBV DNA were detected in 10 of the 34 patients without HBsAg and with anti-HCV. HBV DNA was integrated into chromosome 11q in 4 of the 10 HCCs with junctions. The DNA to either side of the human-viral junctions was sequenced. Clinically, the mean tumor size of these 10 HCCs was 39 mm; that of the 24 HCCs without integrated HBV was 25 mm. The surrounding tissue was cirrhotic in 2 of the 10 former HCCs and in 16 of the latter 24 HCCs. In conclusion, integrated HBV was detected in some patients with HCV infection; in these patients, the integrated DNA was associated with accelerated hepatocarcinogenesis. J. Med. Virol. 69:475,481, 2003. © 2003 Wiley-Liss, Inc. [source] | ||||||||||