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)

It has been shown that hepatitis B virus (HBV) X antigen (HBxAg) functioned as a transactivating element which can act on the enhancer of HBV in an in vitro system and elevate the transcriptional level of HBV. In this study we investigate the relationship between HBxAg expression and HBV replication in patients with chronic hepatitis B and cirrhosis. Rabbit IgG against recombinant HBxAg which was synthesized in E. coli were prepared and used for the detection of HBxAg. HBV DNA was amplified by polymerase chain reaction technique by using primers from HBx gene sequence. Liver tissue samples and sera from the patients were examined immunohistochemically for HBxAg and serologically for HBxAg/anti-HBx respectively. We focused on its expression in these samples in comparison with markers of HBV replication. It was found that in liver HBxAg was present in 72.7% of the patients with chronic active hapatitis (CAH) and 92.6% of those with cirrhosis, while the positivity rate of HBcAg in cirrhosis patients was only 47.8%. In the sera of the patients with CAH, chronic persistant hepatitis and cirrhosis HBxAg was present in 44.4%, 66.6% and 33.3% respectively. It was similar to that observed with HBeAg. Moreover in these HBxAg positive sera HBV DNA can also be detected. It was shown that higher rate of positivity of HBxAg was found in patients with replicative markers (serum HBeAg, serum HBV DNA or liver tissue HBcAg positive). Our results indicate that expression of HBxAg is closely correlated with HBV replication and HBxAg may be an important marker in chronic HBV infection.
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PMID:[Analysis of hepatitis B virus X antigen expression in chronic hepatitis B and cirrhosis]. 758 1

Hepatitis B virus (HBV) DNA and its 5 antigens were studied in 225 cases of paraffin-embedded sections of human liver cirrhosis obtained by biopsy. HBxAg, pre-S1 and pre-S2 antigens were detected by immunohistochemical ABC method, HBsAg and HBcAg by PAP method. HBV DNA by in situ hybridization, and both HBV DNA and HBsAg, HBxAg or HBcAg by double labelling technique of immunohistochemistry and in situ hybridization respectively. The results showed that the positive rates were 70.0% (128/183) for HBsAg, 64.4% (85/132) for pre-S1 antigen, 61.4% (81/132) for pre-S2 antigen, 75.3% (113/150) for HBxAg, 22.4% (39/174) for HBcAg and 62.4% (58/93) for HBV DNA respectively. The double labelling positive rates were 37.3% (19/51) for both HBV DNA and HBsAg, 86.3% (44/51) for both HBV DNA and HBxAg and 39.2% (20/51) for both HBV DNA and HBcAg respectively. More than 80% of the cases with positive sections for HBV DNA and its 5 antigens were associated with liver cell dysplasia (LCD). The results of this study suggest that the occurrence and development of liver cirrhosis were closely related to chronic infection of HBV in China.
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PMID:[Expression and significance of HBV DNA and its 5 antigens in liver cirrhosis]. 778 Nov 8

The expressions of c-erbB-2 oncogene and epidermal growth factor receptor (EGFR) were investigated immunohistochemically in specimens from 184 cases of hepatitis B, cirrhosis and hepatocellular carcinoma (HCC) and 29 normal liver specimens. EGFR was expressed in 36% (48/134) of the hepatocellular carcinoma and chronic liver disorder specimens and it was immunolocalized mainly in the sinusoidal endothelial cells. No significant difference was found between EGFR expression in HCC and in benign chronic liver disorders. These results indicate that EGFR may have some role in the proliferation of the sinusoidal epithelial cells in chronic liver disease. Low level c-erbB-2 expression was observed in 5/29 (17%) of normal liver specimens. In chronic hepatitis B and liver cirrhosis, its expression was found in all specimens. c-erbB-2 protein was immunolocalized mainly in small polygonal liver cells (SPLCs) and hepatocytes in small-cell dysplasia (SCD) and in ductular metaplasia (DM); c-erbB-2 expression in HCC cells was found to be weaker than in SPLCs, the hepatocytes in SCD and in DM. These results indicate that activated c-erbB-2 oncogene may have a role in human HCC genesis through promoting the development of SCD from SPLC proliferation and the progression of SCD. The close relation between the expression of c-erbB-2 and HBxAg imply that the activation of c-erbB-2 in human liver tissues may be related to HBV X gene.
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PMID:[Expression of c-erbB-2 protein and EGF receptor in hepatitis B, cirrhosis and hepatocellular carcinoma]. 778 35

A mouse monoclonal antibody directed against hepatitis B virus (HBV) X protein (HBxAg) was prepared. The antibody was used to screen by immunohistochemistry 50 liver tissue sections from patients with hepatocellular carcinoma (HCC), and 15 patients with chronic active hepatitis (CAH). 28 of 50(56%) samples were HBxAg positive in tumor tissues. The positive rates of HBxAg only in tumor tissues or in adjacent nontumor tissues were 24% and 16%. HBsAg was detected in 16% of cases in tumor tissues and 74% in surrounding nontumor tissues. In CAH samples, the positive rates of HBxAg and HBsAg were 6.6% and 73.3%. HBcAg was only detected in nontumor surrounding liver tissues, the positive rates being 18%. In CAH samples, no HBcAg was detected. The results showed that HBxAg is a common marker in liver tissue from patients with HBV-related HCC. The findings of HBxAg in the absence of detectable HBsAg and HBcAg in the liver tissues suggested that HBxAg could be independent of HBV replication and implied that the synthesis of HBxAg may be directed from integrated HBV DNA templates. It is possible to use antiHBx monoclonal antibody as a carrier for the targeting therapy of HCC.
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PMID:[Preparation of monoclonal antibody directed against hepatitis B virus X protein and detection of reactive antigen in hepatocellular carcinoma]. 784 49

The case of a young female patient with chronic active hepatitis B, vasculitic purpura, edema, and circulating immune complexes due to mixed cryoglobulinemia is described. Serum transaminases were elevated. Serological assays showed hepatitis B surface antigen (HBsAg), antibody to hepatitis B e antigen (anti-HBe), and antibody to hepatitis B core antigen (anti-HBc) antibodies but no antibody to hepatitis C virus (anti-HCV) or antibody to hepatitis delta virus (anti-HDV) antibodies. Using hepatitis B virus-polymerase chain reaction (HBV-PCR) and direct sequencing a precore/core (preC/C) mutant unable to synthesize HBeAg was detected in serum. HBV antigens were demonstrated in the circulating immune complexes. Following 1 month of treatment with interferon-alpha 2b3 miu three times weekly, alanine aminotransferases returned to normal levels while cryoglobulins and immune complexes disappeared from serum. In addition, 2 months after the onset of treatment serum HBV-DNA was no longer detectable by PCR. Prior to treatment the analysis of cellular immune reactions of peripheral blood mononuclear cells showed a major proliferative response to HBcAg, preS1Ag and HBxAg and a minor response to HBeAg and HBsAg. One month after conclusion of treatment a decline in T-cell reactivity against all HBV antigens was observed. During clinical response to the therapy, however, a strong proliferative response of T cells to HBcAg and HBeAg was demonstrated. In conclusion, immune complex disease may complicate chronic hepatitis B in patients expressing HBe-minus HBV mutants. Treatment with interferon-alpha was found to be effective in mixed cryoglobulinemia even in the presence of HBe-minus HBV mutants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mixed cryoglobulinemia type II in chronic hepatitis B associated with HBe-minus HBV mutant: cellular immune reactions and response to interferon treatment. 789 64

Surgical specimens of 20 cases of human intrahepatic cholangiocarcinoma (n = 12) and cholangiohepatocarcinoma (n = 8) were studied immunohistochemically by ABC technique for HBxAg, pre-S1 and pre-S2 and by PAP method for HBsAg and HBcAg. The neighboring liver tissues with chronic hepatitis or cirrhosis surrounding the tumor were also examined in 19 cases. Of the cancerous tissues, 15 were positive for HBxAg (75%), 8 positive for pre-S1 and pre-S2 (40%), respectively and 2 for HBsAg (10%). Sixteen of 19 liver tissues surrounding the tumor were also positive for HBxAg (84.2%), 9 for pre-S1 and pre-S2 each (47.4%), 6 for HBsAg and HBcAg each (31.6%). The results suggest that a close relationship exists between cholangiocarcinoma and cholangiohepatocarcinoma and hepatitis B virus infection. The HBxAg might play an important role in the pathogenesis of cholangiocarcinoma.
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PMID:[Expression of five different antigens of HBV in human intrahepatic cholangiocarcinoma and cholangiohepatocarcinoma]. 817 60

Monoclonal antibodies recognizing the stable imidazole ring-opened form of the major N7-guanine aflatoxin B1-DNA adduct have been used in competitive enzyme-linked immunosorbent assays (ELISA) and indirect immunofluorescence assays to quantitate adduct levels in liver tissue. Methods were developed in AFB1-treated animals, then applied to paired tumor and nontumor liver tissues of hepatocellular carcinoma patients from Taiwan. An avidin-biotin complex staining method was also used for of the detection of hepatitis B surface (HBsAg) and X (HBxAg) antigens in liver sections. A total of 8 (30%) hepatocellular carcinoma (HCC) samples and 7 (26%) adjacent nontumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent nontumorous liver samples were positive, and 9 (33%) HCC samples and 11 (41%) adjacent nontumor liver samples were HBxAg positive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These methods should be useful in determining the role of exposure in the induction of HCC in Taiwan.
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PMID:Immunohistochemical detection of aflatoxin B1-DNA adducts and hepatitis B virus antigens in hepatocellular carcinoma and nontumorous liver tissue. 839 34

Hepatitis B virus (HBV) is one of the most important causes of chronic liver disease. HBV is a DNA virus with an external glycoprotein surface and an internal nucleocapsid which contains the viral genome. HBV infection is revealed by the appearance of specific markers. Some of these markers are well known and their presence in serum is important to understand the behaviour of the disease. Among them HBsAg, HBeAg, anti-HBs and anti-HBe are found in serum, so as anti-Core; the HBcAg may be found in hepatic tissue and marks infectivity and virus replication. In the few last years some new antigens and antibodies have been studied and their importance in diagnosis and follow-up of hepatitis has been recognized. HBxAg, Pre-S and DNA-Polymerase (Pol) seem to be specific and early signals of viral replication. More studies showed the trans-activating properties of HBxAg; actually the X protein seems to be involved in replicative cycle of HBV. Many Authors also demonstrated a relationship between the presence of X in serum and/or liver and the progression of disease to cirrhosis and hepatocellular carcinoma. The Pol antigen and its antibody seem to be very common markers of HBV infection in serum of patients with hepatitis. Moreover their presence is the only signal of viral infection in some patients which have no other marker of HBV. More studies are of course needed to exactly establish the significance of these new markers and their importance for diagnosis and prognosis of HBV infection.
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PMID:[Hepatitis B virus: new markers and their immunology]. 848 26

A series of antisense phosphorothioate oligodeoxynucleotides against hepatitis B virus (HBV) were synthesized and evaluated for their antiviral effect in Hep-G2 cells transfected with HBV genome. The inhibitory effect of the tested antisense oligonucleotides was sequence-specific, dose-and time-dependent, and synergistic for certain combinations. In virus-inhibitory concentrations the oligonucleotides were harmless to 2.2.15 cells. The most effective antisense oligonucleotides were found directed against the HBV mRNA transcribed from the cap site of SP II promoter, the portion of polyadenylation signal and the initiation region of gene S, with an inhibition of the HBsAg and HBeAg production by 85-95% and 50- 60%, respectively. To our surprise, antisense oligonucleotides directed against three key sites of HBV X gene blocked the expression of HBsAg, HBeAg and HBxAg. This fact might be related to the trans-activation of HBV X protein. Using radioisotope labelling, we demonstrated that Lipofectin promoted the cellular uptake and antiviral effect of antisense oligomers in 2.2.15 cells. These results suggest a therapeutic potential of antisense oligonucleotides in the treatment of patients chronically infected with HBV.
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PMID:Inhibition of hepatitis B virus in vitro by antisense oligonucleotides. 888 96

It has been reported that the products of the human hepatitis B virus (HBV) X genes can transactivate a variety of viral and host promoters including the X, core, pre S2/S and pre S1 promoter. In order to investigate their antiviral effect in cell culture, three pieces of antisense phosphorothioate oligodeoxynucleotides (ASON) complementary to HBV X genes 1510-1530, 1555-1581, 1768-1791 regions were synthesized. The specificity of the inhibitory effect of the ASON was determined by using 2, 2, 15 cells by ELISA, PAP-ELISA and in situ hybridization to detect HBsAg, HBeAg, HBxAg and HBV DNA. The results showed that these ASON could inhibit the expression of HBxAg, as well as HBsAg and HBeAg, with the inhibitary rates of 78.07%, 80.65% and 62.76% respectively. In situ hybridization results indicated that HBV DNA replication can also be inhibited. The decrease in virus production and the ammount of HBV DNA were dose and time dependent. The mechanism of action may be due to the inhibition of HBxAg by sequences specific to ASON, and then the decrease of its transactivating effect for HBV DNA promoter.
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PMID:[Antiviral effect of antisense oligodeoxynucleotides complementary to hepatitis B virus X gene in vitro]. 1037 87


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