Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe novel peptide-protein microarrays, which were fabricated using semicarbazide glass slides that permitted the immobilization of glyoxylyl peptides by site-specific ligation and the immobilization of proteins by physisorption. The arrays permitted the simultaneous serodetection of antibodies directed against hepatitis C virus (HCV core p21 15-45 peptide, NS4 1925-1947 peptide, core, NS3, NS4, and mixture of core, NS3, NS4, and NS5 antigens), hepatitis B virus (HBc, HBe, and HBs), human immunodeficiency virus (Gp41 and Gp120 for HIV-I and Gp36 for HIV-II), Epstein-Barr virus (VCAp18 153-176 peptide), and syphilis (rTpN47 and rTpN17) antigens using an immunofluorescence assay. Peptide-protein microarrays displayed high signal-to-noise ratios, sensitivities, and specificities for the detection of antibodies as revealed by the analysis of a collection of human sera referenced against these five pathogens.
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PMID:Peptide-protein microarrays for the simultaneous detection of pathogen infections. 1502 26

Hepatocellular carcinoma (HCC) is the most important primary hepatic cancer, being a common cancer type worldwide. Many aetiological factors have been related with HCC development, such as cirrhosis, hepatitis viruses and alcohol. Chronic infection with hepatitis B (HBV) and C viruses (HCV) often results in cirrhosis and enhances the probability of developing HCC. The underlying mechanisms that lead to malignant transformation of infected cells, however, remain unclear. HBV is a DNA virus that integrates into the host genome, and this integration is believed, in part, to be carcinogenic. Besides, the virus encodes a 17 kDa protein, HBx, which is known to be a causative agent in the formation of HCC. On the contrary, HCV is a RNA virus that does not integrate into the host genome but likely induces HCC through host protein interactions or via the inflammatory response to the virus. Products encoded in the HCV genome interfere with and disturb intracellular signal transduction. Some HCV proteins, such as the core protein, NS3 and NS5A, have seen to have a regulatory effect on cellular promoters, to interact with a number of cellular proteins, and to be involved in programmed-cell death modulation under certain conditions. The identification of these proteins functions in HCC development and the subsequent development of strategies to inhibit protein-protein interactions may be the first step towards reducing the chronicity and/or of the carcinogenicity of these two viruses.
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PMID:Hepatocellular carcinoma: role of hepatitis B and hepatitis C viruses proteins in hepatocarcinogenesis. 1535 43

The purpose of this study was to explore the relationship between hepatitis C virus (HCV) infection and glomerulonephritis. Renal autopsy tissues taken from 21 patients with HCV infection were examined by immunohistochemical technique (S-P assay) with monoclonal anti-HCV NS3 and anti-HCV NS5. Results showed that HCAg positivity were detected in 13 out of 21 renal tissues (61.9%). 11 and 1 out of 13 were identified as membranoproliferative glomerulonephritis (MPGN) and mesangial proliferative glomerulonephritis (MsPGN) respectively, and another 1 case did not show obvious lesion. 8 out of 21 cases were negative for HCAg, in which MsPGN and membranous glomerulonephritis (MN) as well as postinfectious glomerulonephritis (PSGN) were identified in 2 and each in 1 case, respectively, except another 4 cases with no obvious lesion. The renal lesion were more common and diverse in HCV associated glomerulonephritis than hepatitis B virus (HBV) associated glomerulonephritis, the show of clinical data were similar between the two. There was HCV related glomerulonephritis and the clinical manifestation may present relevantly.
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PMID:[Glomeruli manifestation of hepatitis C virus infection]. 1561 41

This study was designed to evaluate the seroprevalence of hepatitis G virus (HGV) infection, its impact, and its relationship with other hepatotropic viruses among chronic renal failure patients undergoing hemodialysis at the Lok Nayak Hospital, New Delhi. The study group consisted of 100 consecutive cases of patients with chronic renal failure undergoing hemodialysis and equal healthy controls matched for age and sex. The patients were included on the basis of detailed history, clinical examination, and liver function profile. HGV RNA was detected in serum samples of all patients as well as of healthy controls using nested reverse transcription polymerase chain reaction (RT-PCR). The primers used were derived from the NS3 helicase region of the viral genome. Serological assay was used for screening the viral markers for hepatitis B and C (HbsAg and Anti HCV). A history of blood transfusion was recorded in 65% of the cases. HGV RNA was detected in only six out of 100 (6%) cases of chronic renal failure. The seroprevalence of HCV infection was detected in 27 (27%), while HBV infection was seen in 10 (10%) out of 100 cases. The mixed infection of HGV and HCV was seen in 33.3% (two out of six) of the chronic renal failure cases, while the coinfection between HGV and HBV was not observed. In the 100 cases of healthy controls, HGV RNA was detected in only three (3%) subjects. Serological markers for Anti HCV antibody and HbsAg were positive in only one (1%) and two (2%) of the subjects, respectively. The seroprevalence of HGV infection in chronic renal failure was found to be statistically nonsignificant when compared to that of healthy controls. Also, there was no difference in clinical course and liver function profile of HGV-positive and HGV-negative cases. However, alanine aminotransferase (ALT) was significantly out of range in HCV-positive patients compared with HCV-negative patients. The presence of HGV infection reflected a postparental exposure to blood and blood-contaminated products in hemodialysis patients. It is suggested that HGV infection in cases of chronic renal failure is unlikely to influence the course of the disease and may be considered an innocent bystander.
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PMID:Hepatitis G virus infection in hemodialysis patients from urban Delhi. 1571 40

BILN-2061, a specific and potent peptidomimetic inhibitor of the HCV NS3 protease, has recently been shown to markedly lower serum hepatitis C virus (HCV)-RNA levels in patients chronically infected with HCV genotype 1 in three 2-day proof of principle studies. The aim of the current study was to assess the antiviral efficacy of BILN-2061 in patients with genotypes 2 and 3 HCV infection. The antiviral efficacy, pharmacokinetics, and tolerability of 500 mg twice-daily BILN-2061 given as monotherapy for 2 days in 10 patients chronically infected with non-genotype 1 HCV (genotype 2: n = 3; genotype 3: n =7) and minimal liver fibrosis (Ishak score 0-2) were assessed in a placebo-controlled (placebo n = 2), double-blind pilot study. HCV-RNA levels decreased by > or =1 log(10) copies/mL in 4 of 8 patients treated with BILN-2061. One patient showed a weak response of <1 log(10) copies/mL. Three of 8 treated patients showed no response. There was no correlation between baseline viral concentration or genotype and response. BILN-2061 exhibited good systemic exposure after oral administration and was well tolerated. In conclusion, the antiviral efficacy of the HCV serine protease inhibitor BILN-2061 is less pronounced and more variable in patients with HCV genotype 2 or 3 infection compared with previous results in patients with HCV genotype 1. A lower affinity of BILN-2061 for the NS3 protease of genotypes 2 and 3 HCV is most likely a major contributor to these findings.
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PMID:Antiviral efficacy of NS3-serine protease inhibitor BILN-2061 in patients with chronic genotype 2 and 3 hepatitis C. 1573 92

Hepatitis virus infection, especially type C (hepatitis C virus [HCV]), has been suggested to be one of the important pathogenetic factors for low- and high-grade B-cell lymphoma, including splenic marginal zone lymphoma (SMZL), in southern Europe. Here, we analyzed the incidences of HCV and hepatitis B virus (HBV) infections, and the clinicopathologic features in 29 cases of splenic diffuse large B-cell lymphoma (DLBCL), 10 SMZL, 3 splenic mantle cell lymphoma, 1 hairy cell leukemia, 13 B-chronic lymphocytic leukemia, and 12 hepatosplenic T-cell and natural killer cell lymphoma. Fifteen (51.7%) splenic DLBCL cases were HCV antibody-positive, and another 6 (20.7%) had the HBsAg. The incidence of each was significantly (P < .01) higher than those of HCV (9.3%) and HBV (1.9%) infections in 54 node-based DLBCL cases. Four examined HCV-positive DLBCL cases showed no type II cryoglobulinemia. HCV RNA was detected in fresh tumor tissues from 6 of 7 examined DLBCL cases, and HBV DNA was present in another 2, as evaluated by real-time polymerase chain reaction. Immunohistologically, tumor cells in 5 of 7 examined DLBCL cases showed intracytoplasmic reactions for HCV NS3 and E2 proteins and the viral receptor CD81. Of 6 cases, 2 showed an intranuclear reaction for the HBV surface protein. By Southern blot analysis, no rearrangement of the Bcl2 gene was detected in the tumor tissue of 7 HCV-positive DLBCL cases. For the other types of malignant lymphoma, 1 case each of SMZL (10%) and hepatosplenic T-cell and natural killer cell lymphoma (8.3%) showed HCV infection. In conclusion, persistent human hepatitis virus infections, especially HCV, may play an important role in the tumorigenesis of splenic DLBCL in Japan.
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PMID:Splenic large B-cell lymphoma in patients with hepatitis C virus infection. 1611 4

The major aim of the project was the development of virus-like particles (VLP) displaying B- and T-cell epitopes of hepatitis C virus (HCV) proteins. To this end, hepatitis B virus core (HBc) particles were used as a carrier of HCV epitopes. Fragments of HCV genes encoding core (aa 98) and NS3 (aa 155) proteins were fused to the 3' terminus of the truncated HBV core gene. All recombinant plasmids led to relatively high levels of expression of chimeric proteins in E. coli, which resulted in the formation of complete "mature" VLP. Chimeric HBc/HCV VLPs were purified by combination of gel filtration and sucrose gradient centrifugation, and used for immunogenicity studies in mice. All variants of hybrid particles induced high humoral and cellular responses to HBcAg. Immunization with the HBc/HCV core particles led to relatively low antibody and T-cell proliferative responses to HCV core epitopes. The HBc/HCV NS3 particles were able to induce high levels of anti-NS3 antibodies in the absence of proliferative responses to HCV epitopes. Thus, the results of the current study have demonstrated the principal possibility of using VLP on the basis of HBcAg for creation of a new type of HCV-specific immunogen.
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PMID:Recombinant virus-like particles as a carrier of B- and T-cell epitopes of hepatitis C virus (HCV). 1657 85

Essential data pertaining to the structure and function of selected transcription factors such as NFAT, AP-1 and NF-kappaB in particular, are presented in the relation to viral hepatitis C and B. In chronic hepatitis C the activation of NF-kappaB is markedly modulated by viral proteins such as core protein and nonstructural ones, particularly NS5A and NS3. In hepatitis B the major factor influencing NF-kappaB function appears to be HBx protein. Effects of viral proteins on NF-kappaB function in relation to the course of hepatitis are complex. They participate in the perpetuation of inflammatory state in the liver, inhibit apoptosis of hepatocytes, as well as the differentiation of antigen-presenting cells (dendritic ones). The latter effect has deleterious impact on the formation of specific immune response to viral peptides. It seems that both viruses, C and B acquired the ability to modify NF-KB function in advantage for the pathogens in question.
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PMID:[The role of NF-kappaB transcription factor in chronic viral hepatitis C and B]. 1686 2

Hepatocellular carcinoma (HCC) is a fatal disease and hepatitis B and C viruses (HBV and HCV) are considered as major causative factors for the development of HCC. We have conducted gene expression profiling studies to search for potential target genes responsible for HCV-mediated HCC. Adenoviruses encoding core (HCV structural protein), NS3 and NS5A [HCV non-structural (NS) proteins] were generated and infected individually or together in freshly isolated primary human hepatocytes. An adenovirus harboring the oncogenic HBV protein, HBx, was included for comparison. A microarray platform of over 22,000 human oligos was analyzed to seek out significant differentially expressed genes among these viral proteins. We also compared these gene expression profiles with those obtained from HCV-infected liver samples from chronic liver disease (CLD) patients and HCV-related HCC. We found that HCV-related proteins largely induce unique genes when compared with HBx. In particular, interferon-inducible gene 27 (IFI27) was highly expressed in HCV or core-infected hepatocytes and HCV-related CLD or HCC, but was not significantly expressed in HBx-infected hepatocytes or HBV-related CLD or HCC, indicating that IFI27 may play a role in HCV-mediated HCC. In conclusion, our results suggest that HBV and HCV promote HCC development mainly through different mechanisms.
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PMID:Induction of a unique gene expression profile in primary human hepatocytes by hepatitis C virus core, NS3 and NS5A proteins. 1740 95

Several studies have suggested an association between Hepatitis C and B viruses (HCV and HBV) and non-Hodgkin's lymphoma (NHL). In the present study we have searched for viral genomes and antigens in the malignant lymphoma tissues as well as their seroprevalence. Antibodies against Hepatitis C as well as HCV RNA and hepatitis B surface antigen (HBsAg) were determined for 29 newly diagnosed non-Hodgkin's lymphoma patients using an enzyme linked immunosorbent assay (ELISA), as well as RT-PCR and compared with 36 apparently healthy individuals as a control group for viral markers. Immunohistochemical staining (IHC) was performed on paraffin embedded tissues for the NS3 of HCV and for HBsAg of HBV using the immunoperoxidase technique. Paraffin embedded lymph nodes (LN) were studied for the presence of viral sequences. Ten non-metastatic lymph nodes (LN) from cancer cases other than NHL were used as a control for IHC and molecular studies. HCV was significantly more encountered in patients with NHL when compared to controls for both antibodies (27.6% versus 8.3% of serum controls; p = 0.04), and antigens studied by IHC in the involved LN (41% versus 10% of tissue controls; p = 0.06). Although HBsAg positivity was not different in NHL patients when compared to controls (6.9% and 2.7%); yet it was significantly more encountered in LN of NHL patients (p = 0.04). HBV-DNA was detected in 27.5% of patient's samples and none of the controls. In conclusion, overall our findings confirm the presence of HBV and HCV antigens and viral sequences in the involved LNs of NHL patients, except for HCV RNA which perhaps necessitates fresh and not paraffin embedded tissues. These results strengthen the assumption that these viruses may be involved in the development of NHL.
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PMID:Viral genomes and antigen detection of hepatitis B and C viruses in involved lymph nodes of Egyptian non-Hodgkin's lymphoma patients. 1797 55


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