ad and ay subtypes of hepatitis B antigen in a case of hypogammaglobulinaemia.
(25/499)
We describe the finding of d and y specificities of hepatitis B surface antigen (HBsAg) in a case of hypogammaglobulinaemia of the 'common variable' type treated with fresh frozen plasma infusions. Absorption studies show that the two specificities are on separate particles, suggesting dual infection. It raises important questions regarding the relationship between HBsAg persistence and the immune status of the carrier. (+info)
Hepatitis B antigen (HBAg) infection in a hemodialysis unit. I. HL-A8 and immune response to HBAg.
(26/499)
A total of 28 hemodialysis patients and 23 healthy individuals working in close association with the patients or their blood samples were found to possess either HBAg (22) or anti-HBAg (29). HL-A typing revealed the lack of HL-AB in the group with anti-HBAg, suggesting that the immune response to HBAg may be negatively associated with HL-AB. (+info)
Activation of the insulin-like growth factor II transcription by aflatoxin B1 induced p53 mutant 249 is caused by activation of transcription complexes; implications for a gain-of-function during the formation of hepatocellular carcinoma.
(27/499)
Aflatoxin B1 (AFB1) induced mutation of the p53 gene at codon 249 (p53mt249) is critical during the formation of hepatocellular carcinoma (HCC) following hepatitis B virus (HBV) infection. p53mt249 markedly increases insulin-like growth factor II (IGF-II) transcription largely from promoter 4, accumulating the fetal form of IGF-II. Modulation of the transcription factor binding to IGF-II P4 by wild-type p53 and p53mt249 was identified. Wild-type p53 inhibited binding of transcription factors Sp1 and TBP on the P4 promoter, while p53mt249 enhanced the formation of transcriptional complexes through enhanced DNA-protein (Sp1 or TBP) and protein-protein (Sp1 and TBP) interactions. p53mt249 stimulates transcription factor Sp1 phosphorylation which might be a cause of increased transcription factor binding on the P4 promoter while wild-type p53 does not. Transfection of hepatocytes with p53mt249 impaired induction of apoptosis by the HBV-X protein and TNF-alpha. Therefore, the blocking of apoptosis through enhanced production of IGF-II should provide a favorable opportunity for the selection of transformed hepatocytes. These results explain the molecular basis for the genesis of HCC by p53mt249 which was found to be induced by a potent mutagen, AFB1. (+info)
Hepatitis B antigens in serum and liver of chimpanzees acutely infected with hepatitis B virus.
(28/499)
We report the temporal patterns of various immunohistological and serological parameters of acute self-limited hepatitis B virus infection of two chimpanzees, and we provide evidence that the synthesis of hepatitis B core antigen precedes that of hepatitis B surface antigen. Our data suggest that existence of a biphasic hepatitis B virus infection involving a hematogenous reinfection of the liver and indicate that recruitment of liver cells to produce hepatitis B virus may occur in a pattern consistent with a replicative cycle of about 8 days. (+info)
The use of fresh frozen plasma or a concentrate of factor IX as replacement therapy before liver biopsy.
(29/499)
Thirty patients with various types of chronic liver disease and a prothrombin time prolonged for four or more seconds who required needle liver biopsy for diagnostic purposes were given either fresh frozen plasma or a concentrate of clotting factors as a prophylactic measure. The prothrombin time returned to within normal limits in seven of the 15 patients given the concentrate and in three of those receiving fresh frozen plasma. Levels of factors II, IX, and X showed increases of about 30% following concentrate administration; corresponding rises in the group given fresh frozen plasma were less. This was because of the smaller quantity of clotting factors administered with fresh frozen plasma and the increase in factor II and IX activity/kg body weight/unit of clotting factor injected was greater when fresh frozen plasma was used. In neither group was there clinical evidence of bleeding, but it was of interest that most of the clotting factor levels, except in factor II, before biopsy were above those normally required for haemostasis. No evidence of disseminated intravascular coagulation was found with the concentrate injection, and the most worrying finding was the appearance of HBAg some months later in three patients, two from the concentrate group and one from those given fresh frozen plasma. However, the conversion of these patients to HBAg positive may be unrelated to the clotting factor replacement therapy. (+info)
Hepatitis B surface antigen (HBsAg) infection in a hemodialysis unit. II. Factors affecting host immune response to HBsAg.
(30/499)
Serum from 86 hemodialysis patients, 105 healthy hospital staff "at risk" and 160 regular hospital staff was screened for hepatitis B surface antigen (HBsAg) and antibody (anti-HBs). The combined prevalence of HBsAg and anti-HBs was higher in the staff of the artificial kidney unit (57.7%) than in the hemodialysis patients (33.7%). The healthy subjects with HBsAg infection responded significantly more often by producing anti-HBs compared with the hemodialysis patients. Twelve of 29 (41.4%) hemodialysis patients with HBsAg infection produced anti-HBs, while 17 (58.6%) remained positive for HBsAg. This differential response could not be attributed to age, sex, time spent undergoing hemodialysis, delayed cutaneous reactivity or response to phytohemagglutinin (PHA) or pokeweed mitogen (PWM). However, a much larger proportion of patients with HBsAg than with anti-HBs had previously received blood transfusions (88.2% v. 33.3%). Our results indicate that development of the chronic HBsAg carrier state or production of anti-HBs in uremic patients may be influenced by the route of immunization or the dose of antigen, or both. Although uremic patients maintain normal in vitro response to PHA and PWM, they may have depressed immunity in vivo because of a decreased total number of T-lymphocytes. (+info)
Characterization of 'e' antigen associated with hepatitis B.
(31/499)
Hepatitis B 'e' antigen (HBe) from the serum of a chronic carrier of HBsAg has been partially purified and characterized. It behaves as an acidic protein, pI 4.5--5.0, which is thermolabile and sulphydryl-sensitive. In serum it usually has a flotation density 1.3 g/cm3, but is sometimes found at density 1.15 g/cm3 because of its association with lipid. HBe from serum is polydisperse on gel filtration although most antigen is recovered with a nominal molecular weight of 3 x 10(5) Daltons. In contrast, in the presence of chaotropic ions, the bulk of serum HBe is found as a species of 3 X 10(4) Daltons previously detected in small amounts under non-dissociating conditions. This suggests that the larger material is formed by non-covalent association of the 3 X 10(4) Dalton species either with itself or other serum components. This would include IgG, although there is no evidence that HBe itself bears immunoglobulin determinants. Analysis of HBe precipitins by polyacrylamide gel electrophoresis under reducing and dissociating conditions suggests that its component polypeptide chains are about 1.7 X 10(4) Daltons. (+info)
Chemotherapeutic drug, adriamycin, restores the function of p53 protein in hepatitis B virus X (HBx) protein-expressing liver cells.
(32/499)
Hepatitis B virus X (HBx) protein implicated in the development of liver cancer may inhibit the function of p53 tumor suppressor protein through cytoplasmic retention of p53 protein. Here, we attempt to investigate whether the functional inhibition of p53 protein by HBx protein is reversible. First, we provide the evidence for the association of endogenous p53 protein with HBx by co-immunoprecipitation in stable Chang cells that express HBx protein in an inducible manner (ChangX-34). By immunofluorescence microscopy, the major location of p53 protein of ChangX-34 cells was confirmed at the nuclear periphery as well as in the cytoplasm where HBx protein is mainly expressed. Surprisingly, anticancer drug, adriamycin induces the nuclear translocation of p53 protein sequestered in the cytoplasm. This change is accompanied by the restoration of p53 activity, which results in increased transcriptional activity at the p53-responsive DNA elements as well as increase of p21WAF1 mRNA expression. Further, we observed the induction of cell death and G1 arrest in these cells upon adriamycin treatment regardless of HBx expression. Together, we demonstrate that functional inhibition of p53 protein through its cytoplasmic retention by HBx protein is reversible. These results may be extended into other tumors of which p53 activity is modulated by viral oncoproteins. (+info)