Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The function of the X gene was clarified by examination of the transient production of hepatitis B virus (HBV) particles by transfected recombinant HBV DNA (pHBV-3 DNA) and its frameshift mutant (delta X) of the X open reading frame into hepatocellular carcinoma HuH-7 and HepG2 cells. No reduction of viral mRNAs was observed in the HuH-7 cells by the delta X mutant, whereas mRNAs underwent marked reduction in HepG2 cells. No reduction in core particle production was observed in HuH-7 cells, but in HepG2 cells reduction was considerable. To clarify the significance of the delta X mutation in the trans-acting function of the X gene in hepatoma cells, the chloramphenicol acetyl/transferase (CAT) assay was conducted. Transfection of plasmid pHBV-3 into HepG2 cells increased CAT activity of pSV2-CAT, while the delta X mutation clearly showed no stimulation of activity. On the other hand, in the HuH-7 cells, pHBV-3 exhibited no such stimulation. The trans-acting function of the X gene product in two different hepatoma cells was clearly shown to differ. Furthermore, transfection of X gene expression plasmid pKSV-HBx into mouse NIH3T3 cells increased the CAT activity of pSV2-CAT. Trans-activation was still detectable even following deletion of enhancer sequences in the pSV2CAT. The oncogenic potential of HBV is discussed with special attention to the X gene product, which may be able to activate a cellular transcription factor at the viral and cellular promotor sequences in the cells.
Mol Biol Med 1989 Apr
PMID:Oncogenic potential of hepatitis B virus. 261 44

Proteins of either HIV-1, hepatitis B, or rabies virus were incorporated with the adjuvant substance Quil A and cholesterol into the immunostimulating complex: iscom. Formation and symmetry of this regular complex were analyzed by electron microscopy. Micellar structures with a diameter of about 12 nm, occasionally with a 7-nm stain-filled center, were formed in a 0.03% water suspension of Quil A. Cavities or holes appeared in the smooth structures of cholesterol upon the addition of Quil A, and after mixing Quil A and cholesterol 1:1 fragile and flattened structures of matrix were produced with a diameter of about 40 nm. By freeze-drying the matrix was preserved as a cage-like, isometric particle. Stable iscom particles composed of Quil A, cholesterol, and selected viral proteins had an approximate diameter of 32 nm. The particles had an uniform, cage-like structure, exhibiting icosahedral symmetry, irrespective of the viral proteins incorporated. Tilting experiments and rotational image analysis indicated that the iscoms were composed of 20 morphological subunits assembled in a pentagonal dodecahedron with a hole on each of the 12 pentagonal faces. The symmetrical shape of the iscom might explain both its remarkable stability and its capacity to efficiently present antigens to the immune system.
J Ultrastruct Mol Struct Res 1989 Dec
PMID:Quaternary structure of the immunostimulating complex (iscom). 263 9

In order to study aspects of the biology and pathogenesis of the hepatitis B virus (HBV), not readily approachable by existing tissue culture systems and animal models, several groups have introduced the HBV genome and subgenomic fragments into the germ line of transgenic mice. Substantial new information has been forthcoming from these studies in several areas including tissue-specific expression, hormonal regulation, sex influences, viral replication and disease pathogenesis. These developments are reviewed in the context of the genetic organization and functional properties of the virus and its gene products, and their implications with respect to HBV biology and pathogenesis are discussed.
Mol Biol Med 1989 Apr
PMID:Hepatitis B virus gene expression in transgenic mice. 269 89

The pathogenesis of hepatitis B virus (HBV) infection is variable and can result in the development of acute and chronic hepatitis, cirrhosis and primary hepatocellular carcinoma (PHC). In this review, the relationship between the patterns of virus gene expression, host immunological responses, and liver pathology in chronic infection will be discussed. Available evidence suggests that the virus is not directly cytopathic to liver cells and that the pathologic sequelae to infection are mediated by both humoral and cellular immune responses against one or more virus gene products. In addition, chronic liver disease might also be mediated by autoaggressive immune responses that may be stimulated by the direct action of virus gene products upon host gene expression, by the lysis of infected hepatocytes by virus specific host immune responses, or by both. Given the complex and variable outcome of HBV infection, the lack of adequate treatment for chronic liver disease, and the fact that long-term infection dramatically increases the risk of developing PHC, the future provides challenges for devising new models to study, understand and successfully manipulate the pathogenesis of chronic HBV infection.
Mol Biol Med 1989 Oct
PMID:Hepatitis B virus gene products as immunological targets in chronic infection. 269 58

An 83-base-pair-long hepatitis B virus DNA fragment efficiently activates the transcription of the heterologous globin gene promoter. This fragment contains binding sites for at least four distinct cellular factors termed E, TGT3, EP, and NF-I. E is a positively acting factor, responsive to phorbol ester. EP is apparently identical to the factor EF-C that binds to the polyomavirus enhancer. The conservation of the binding site sequences for most of these factors in the genomes of other members of the hepadnavirus family suggests that these viruses share common enhancer elements.
Mol Cell Biol 1989 Apr
PMID:Cellular factors that interact with the hepatitis B virus enhancer. 272 24

The presence of hepatitis B virus (HBV) and human immunodeficiency virus (HIV) was investigated using hybridization in 15 lymph nodes and one Kaposi's sarcoma skin lesion obtained from HIV-positive patients. Cryostat tissue sections were hybridized with chemically modified DNA probes for HBV and HIV. HIV genome was mainly observed in the cytoplasm of cells present in 7/15 lymph nodes and in the Kaposi's sarcoma skin lesion, thus indicating the expression of HIV replication. Control samples hybridized with an HTLV I probe were negative. HBV genome was found in the cytoplasm of lymphoid mononuclear cells in 2/7 lymph nodes, obtained from HIV+ patients without serum markers of ongoing HBV infection. Lymph node positivity for HBV DNA also confirms that lymphoid cells may be a target for HBV. Since HBV infection seems to precede HIV infection in nearly all patients, it is possible that it may represent a factor facilitating the development of the HIV-related disease.
Mol Cell Probes 1989 Jun
PMID:HBV and HIV expression in lymph nodes of HIV positive LAS patients: histology and in situ hybridization. 277 Jul 52

The envelope protein of hepatitis B virus carrying the surface antigen, HBsAg, has the unique property of mobilizing cellular lipids into spherical or elongated particles, about 22 nm in diameter, which are secreted from mammalian cells. We have created mutant envelope proteins by insertion of various sequences of different lengths into two regions of the S gene encoding the major envelope protein. S genes carrying inserts in phase with HBsAg were expressed in mouse L cells from the simian virus 40 early promoter. Various single or double inserts in the two major hydrophilic domains of HBsAg were compatible with secretion of 22-nm particles. In all mutant envelope proteins studied, the HBsAg domains required for intracellular aggregation appeared to be intact. However, assembly into particles was not sufficient to assure transport into the extracellular space. The 22-nm HBsAg particle may be a useful vehicle for the export and presentation of foreign peptide sequences.
J Mol Biol 1987 May 20
PMID:Insertions in the hepatitis B surface antigen. Effect on assembly and secretion of 22-nm particles from mammalian cells. 282 Dec 75

Sera from children bearing embryonal tumors and from their parents were screened for the presence of hepatitis B virus (HBV) and its DNA by means of serology and molecular hybridization, respectively. Sera from tumor-bearing children and their parents both contain HBV or its DNA at average 5 times more frequently than the healthy donors or patients with non-oncological diseases. It is suggested that the presence of HBV or its DNA is caused not solely by infection during cure but also by vertical transmission from parents. The presence of HBV or its DNA might be treated as a risk factor increasing the development of embryonal tumors.
Mol Biol (Mosk)
PMID:[Hepatitis B virus and the development of human embryonal tumors]. 283 18

Eight liver biopsy specimens from five patients with PAS-negative intracisternal hyalin were investigated by immunofluorescence for: (1) immunoglobulins (Ig) G, A, M, D, E; (2) light chains (kappa and lambda); (3) complement components C1q, C4, C3c, C5, C9; (4) C1-inactivator; (5) C3-activator; (6) alpha 1-antitrypsin; (7) alpha 1-antichymotrypsin; (8) plasminogen; (9) fibrinogen; (10) fibrinogen breakdown products D and E; (11) fibronectin; (12) prealbumin; (13) albumin; (14) betalipoprotein; (15) apolipoprotein; (16) alpha 1- and alpha 2-glycoprotein; (17) cholinesterase; (18) ceruloplasmin; (19) haemopexin; (20) myoglobin; (21) placenta lactogen; (22) transferrin; (23) actin; (24) myosin; (25) cathepsin D; and (26) hepatitis B surface and core antigens (HBsAg and HBcAg). The globules reacted significantly with antisera against C3c (three patients), C4 (three patients), C3-activator (one patient) and fibrinogen (two patients). The cause of the protein accumulation is not clear. Serial studies indicate the possibility of a disturbance of protein secretion and an as yet unidentified immune complex disorder.
Virchows Arch B Cell Pathol Incl Mol Pathol 1985
PMID:Immunohistological investigations of PAS-negative globular intracisternal hyalin in human liver biopsy specimens. 285 88

Worldwide, primary liver cell carcinoma (PLC) is one of the most common tumours. Epidemiological evidence has implicated hepatitis B virus (HBV) in its aetiology and the mechanisms whereby HBV could operate at the genomic level have been investigated using the techniques of molecular biology. The resemblance of certain features of HBV to the retroviruses has also suggested mechanisms whereby malignant transformation may take place, but as yet there is no clear evidence for HBV being directly oncogenic. This has suggested to some that it is the persistent inflammatory reaction caused by HBV infection that is instrumental in causing PLC. We believe, however, that HBV can act independently of this mechanism and that the failure so far to show this at the molecular level may be due to technical reasons.
Mol Biol Med 1986 Jun
PMID:Hepatitis B virus and primary liver cell carcinoma. The application of molecular biology. 294 50


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