Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis C virus (HCV) antigen expression was examined by immunohistochemical staining in liver tissue taken at biopsy from 8 anti-HCV positive patients. Frozen liver sections were stained by indirect immunofluorescence for capsid, E2/NS1, NS3, NS4 and NS5 using polyclonal antibodies raised to synthetic peptides from these regions. The antigens E2 and NS3 were localised in scattered hepatocytes and also in cells within and around areas of inflammation. A weaker signal was observed for NS4 and NS5 and no signal was seen for capsid antigen. No staining was seen in liver tissue from 9 individuals, including 3 hepatitis B virus-positive and 2 hepatitis delta virus/positive patients, who were negative for serological markers of HCV. The specificity of the staining reaction was also confirmed by the lack of staining in HCV-positive liver samples, after the antisera was pre-adsorbed against the specific peptide. Collectively, the data suggests that HCV may not only be hepatotropic but also lymphotropic, and this may be an important factor in the pathogenesis of HCV infection.
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PMID:Localisation of hepatitis C virus proteins in infected liver tissue by immunofluorescence. 768 8

The partial genome sequence of the hepatitis C virus (HCV) was determined in the serum of a Taiwanese patient with chronic community-acquired type C hepatitis. The cDNA fragments synthesized with the HCV RNA as a template were amplified by polymerase chain reaction using specific oligonucleotide primers. The amplified fragments represented the regions coding for the putative core, matrix and envelope proteins as well as the N-terminal amino acid sequence of the nonstructural protein NS1, the partial nonstructural NS3 and NS4 proteins and the region of the partial 5'-end noncoding sequence. The cDNA fragments were cloned and sequenced. Sequence analysis of these clones showed that they share 83.7%, 93.2% and 93.6% similarity at the nucleotide level, and 86.6%, 94.1% and 92.9% homology at the amino acid level, with the previously published American, Japanese and Taiwanese isolates, respectively. Accordingly, the RNA genome we obtained is HCV type II, probably, the predominant subtype in Taiwan.
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PMID:Sequence determination of hepatitis C virus genome isolated from Taiwan. 786 53

Hepatitis C virus (HCV) is a major cause of post transfusion non-A, non-B hepatitis. The virus contains a positive-strand RNA genome comprised of approximately 9,400 nucleotides. HCV E2/NS1 is probably an envelope glycoprotein (E2). The E2 hypervariable domain appears to contain isolate-specific antibody-binding linear epitopes. Recently, comparative sequence analysis of all the complete and partial HCV sequences published to date indicates that known genotypes of HCV can be classified into six basic groups. We report here that the prevalence of HCV-I, HCV-II, and a mixed form are 77.2%, 11.4%, and 11.4%, respectively. Patients with anti-HCV and HCV-RNA positive chronic active hepatitis received 6MU of interferon-alpha or beta everyday for two weeks followed by 6MU thrice a week for 14 weeks. Complete response to interferon treatment was defined as an ALT level normalized within six months after the end of treatment and maintained within the normal limit for an additional six months. Complete response was found in 42.9% of patients treated for 16 weeks. In a six month follow-up of the complete responders, clearance of viremia was observed in 90.3% at the end of interferon treatment and in 71.0% six months after the end of interferon treatment.
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PMID:[Hepatitis C]. 834 54

Hepatitis C virus (HCV) is important to the liver transplant recipient for several reasons. First, chronic HCV infection is a frequent cause of end-stage liver disease in North America and Europe, where the majority of liver transplants are performed. Second, recurrence of HCV after liver transplantation is almost universal so that many liver transplant recipients with and without overt hepatitis are viraemic. Third, HCV infection in the organ donor and/or in the blood transfused in the peri-transplant period make acquisition of HCV possible. Finally, liver transplantation for chronic HCV infection represents a major financial burden to the health-care system in the USA and worldwide. Histological hepatitis not due to HBV or cytomegalovirus (CMV) is present in 14-35% of allografts from patients undergoing liver transplantation, and the majority of this is due to HCV infection. HCV infection recurs post-transplant in almost all patients with pre-transplant infection. Proof that HCV does recur has been provided by the sequencing of the hypervariable domain of the E2/NS1 region. The magnitude of HCV infection is underestimated by using serological assays in this immunosuppressed population. Using the b-DNA assay, HCV-RNA levels have been shown to increase in patients with recurrent infection. The long-term consequences remain to be defined but post-transplantation HCV infection is generally much less devastating than post-transplantation HBV infection, and many patients have clinically silent disease. It is likely that a carrier state exists in immunosuppressed transplant recipients since high HCV-RNA levels occur in the absence of liver damage. In one study, 1, 2 and 3 year patient survival rates were shown to be comparable in patients with chronic active HCV infection and with cryptogenic cirrhosis (94, 89 and 87%, and 84, 84 and 73%, respectively). A more recent study from the University of Pittsburgh which compared the outcome of a larger number of HCV-infected patients (n = 237) with a large number of control patients with non-viral disease (n = 801), showed that indeed HCV infection does impact negatively on both patient and graft survival (1, 2 and 3 year patient survival in the study and control groups of 78, 68 and 66% and 84, 82 and 78%, respectively, P = 0.001). Undoubtedly with time, the full impact of recurrent HCV infection will become apparent, although short-term survival is sufficiently good to warrant continued transplantation of this group of patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hepatitis C and liver transplantation. 852 17

The recent cloning and genomic identification of hepatitis C virus (HCV) by sensitive and specific immune techniques has allowed a better definition of both histopathological and clinical features of the previously not well defined non-A, non-B hepatitis. In this regard, antibodies to different HCV antigens are usually found during infection, even if some of them such as anti-E1 and anti-E2/NS1 have been shown to be associated with significant viraemic levels. Acute hepatitis C is self-limiting in a minority of cases only. Over 60% of acute hepatitis becomes in fact chronic and may progress towards cirrhosis. In about 10% of cases, hepatocellular carcinoma may develop in cirrhotic livers. The occurrence of a strict relationship between immunoresponsiveness and disease activity is suggested by the observation that peripheral blood mononuclear cell (PBMC) proliferation induced by NS3 structure is associated with self-limiting acute hepatitis, while PBMC stimulation by core antigen characterizes chronic C hepatitis. The demonstration of lymphoid aggregates, bile duct lesions, intraportal lymphocyte infiltration, increased adhesion molecule expression and augmented cytokine release clearly emphasizes the involvement of immune-mediated reactions in the development of liver damage, even if a direct cytopathic effect cannot be excluded. Finally, it is likely that HCV may favour, through immune-mediated mechanisms, autoantibody generation and/or the appearance of some extrahepatic autoimmune manifestations during the course of HCV chronic infection.
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PMID:Hepatitis C virus infection. Biological and immunological features. 876 58

We studied the heterogeneity in the E2/NS1 hypervariable region 1 of the hepatitis C virus (HCV) genome in relation to the natural course after infection. The subjects were composed of 38 chronic hepatitis C carriers who had been followed for 9 to 218 months after the onset of non-A, non-B (type C) hepatitis, being tested monthly for serum alanine aminotransferase levels. The complexity of the sequence heterogeneity was assessed by single-strand conformation polymorphism analysis. The quasispecies complexity had no relation to the route of infection, the time from infection and the duration of aminotransferase elevation after the onset. However, it had a significant relationship with the degree of aminotransferase elevation in the course of the disease. The quasispecies complexity was directly correlated with the first peak of serum aminotransferase at the onset (r = .48, P < .01) and the mean aminotransferase levels during the period of persistent aminotransferase elevation (r = .58, P < .01). Twenty-three of the 38 patients were further followed for 24 months with biweekly alanine transaminase (ALT) tests. Their aminotransferase levels remained within the normal range during follow-up, and no significant change was seen in the quasispecies complexity after this asymptomatic period. However among the 23 patients, the quasispecies complexity increased in six cases (26%) and decreased in five (22%). A significant direct relation was seen between changes in the quasispecies complexity and the mean aminotransferase levels during the asymptomatic period (r = .55, P = .01). These findings suggest that the development of the HCV quasispecies nature may be related to the severity of the hepatitis in the course of infection.
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PMID:Relation of disease activity during chronic hepatitis C infection to complexity of hypervariable region 1 quasispecies. 902 61

Hepatitis C virus (HCV), the major causative agent of post transfusion non-A, non-B hepatitis (NANB), had been cloned and expressed. According to the protein sequence of HCV-BK and its epitope profiles which combined the hydrophilicity, accessibility, flexibility, antigenicity, charge distribution and HPLC reserve coefficient of protein using the "Goldkey" computer program, we designed and synthesized the following peptides: P1(475-495), P3(449-468), P4(658-663), P5(645-663), P6(484-489), P7(475-489), P15(655-662), P16(230-237), P17(225-237), P18(1220-1240), P19(1694-1735), P24(1230-1240), P25(1482-1493), P26(384-389), P27(2355-2389). The results of ELISA showed that P6(60% positive results) and P19(63% positive results) testing with PT-HC of Gu An, Hebei province were the major antigens in NS1 and in NS4 region, respectively.
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PMID:[Studies on synthetic peptide. XX: the antigenicity and linear epitope map of synthetic peptide hepatitis C virus]. 986 43

The nucleotide sequences of the putative envelope region (E1) and the junction between the E1 and envelope 2/nonstructural 1 (E2/NS1) region of the hepatitis C virus (HCV) genome are divergent among different genotypes. To characterize them, we introduced a set of nested primers that are conserved among four different genotypes (types I-IV) of HCV for polymerase chain reaction (PCR) amplification. The amplified products include the variable full-length E1 region, and the 5' end of the E2/NS1 region, the so-called hypervariable region-1 (HVR-1). Of 53 patients with histologically confirmed chronic liver disease and HCV viremia, type II virus was the most dominant strain as detected by the PCR genotyping method and the envelope region could be amplified in more than half of them irrespective of their genotypes. The specificity was confirmed by subsequent nucleotide sequence analysis. The positivity of envelope region PCR was not correlated with histologic diagnosis and hepatitis activities in these patients. Our results suggest that the nested primers can amplify the variable E1 and hypervariable 5' end of E2/NS1 of the HCV genome with moderate efficiency, and thus will be useful in future studies of HCV infections. Copyright 1994 S. Karger AG, Basel
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PMID:Detection of Divergent Hepatitis C Virus Envelope Sequences. 1172 20

Parvovirus B19 is the causative agent of erythema infectiosum. In addition, the infection may be associated with other disease manifestations: anemia and aplastic crisis, thrombo- or granulocytopenies; spontaneous abortion or hydrops fetalis in pregnant women; acute and chronic arthritis in adults and children, myocarditis and hepatitis. Both acute and persistent courses of B19-infections have been reported. All patients develop IgG against the capsid proteins VP1 and VP2, the majority of virus neutralizing antibodies that offer life-long protection against reinfections are directed against the VP1-unique region. IgM is mainly directed against VP2-specific epitopes. These antibodies may be present for only a rather short period of two to ten weeks after acute infection. IgG-antibodies against the nonstructural protein NS1 are preferentially found in patients which are unable to eliminate the virus and develop persisting viremia or virus persistence in distinct organs, e.g. synovial fluid, liver, bone marrow.
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PMID:Antibody responses in parvovirus B19 infected patients. 1211 51

Flaviviruses are major arthropod-borne human pathogens responsible for life-threatening encephalitis, hepatitis and haemorrhagic fevers. These enveloped, single-stranded, positive-sense RNA viruses encode a polyprotein precursor of about 3400 amino acids, processed into three structural and seven non-structural proteins. The non-structural glycoprotein NS1 is essential for flavivirus viability. During host-cell infection in vitro, NS1 is found associated with intracellular organelles as a requisite for its role in viral replication, or is transported to the cell surface where it may trigger specific signalling pathways. In addition, a secreted form of the protein is released from flavivirus-infected mammalian cells. We have previously shown that the NS1 protein circulates during the acute phase of the disease in the plasma of patients infected with dengue virus type 1 and have extended our retrospective studies to dengue type 2 and type 3 cohorts, confirming the value of the NS1 antigen as an alternative diagnostic marker. Interestingly, detection of the NS1 protein in yellow fever virus and West Nile virus infections suggests that NS1 secretion is a hallmark of human flavivirus infections. The objectives of our current studies are to define the biological properties of the secreted form of the NS1 protein, to evaluate its possible contribution to viral pathogenesis, and to validate this protein as a candidate target for passive immunoprophylaxis against flaviviruses.
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PMID:Secretion of flaviviral non-structural protein NS1: from diagnosis to pathogenesis. 1731 66


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