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)

Testing of paired serum samples of 12 children with the Wiskott-Aldrich syndrome for the presence of hepatitis B surface antigen (HBsAg) antibody to HB, Ag, and antibody to the hepatitis B core antigen revealed evidence of hepatitis B virus infection in three. None of the three, however, developed overt clinical hepatitis or the chronic HBsAg carrier state. These data suggest that the immunologic defects seen in the Wiskott-Aldrich syndrome permit adequate immune responses to the hepatitis B virus and do not predispose to the chronic HBsAg carrier state.
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PMID:Hepatitis B virus infection in the Wiskott-Aldrich syndrome. 125 11

A novelty of the present studies is the use of alpha 1-antitrypsin (A-1--AT) as an endogenous marker of enteric protein loss. Enteric clearance of alpha 1-antitrypsin was determined in 10 patients with the symptoms of PLE, and in 6 healthy individuals. Alpha 1-Antitrypsin concentration has been assayed in single, random samples of feces collected from 42 patients and 12 healthy individuals (normal values: 1.31 +/- 0.72 mg/g of feces). Markedly increased enteric clearance and A-1-AT concentrations in single, random samples of feces have been found in patients with enteric lymphangiectasis, Crohn's disease, ulcerative colitis, and constrictive pericarditis, slightly lower in coeliac, chronic diarrhoea, nonspecific hemorrhagic colitis, esophagitis, lambliasis, hypogammaglobulinemia, Wiskott-Aldrich syndrome, Rendu-Osler-Weber syndrome, hepatitis in newborn, and Gilbert's disease. Statistically significant positive clearance has been noted (r = 0.997; p less than .001). A single assay of A-1-AT in feces is simple, repeatable, and sensitive technique in the diagnosis and evaluation of these diseases in which the symptoms of enteric protein loss are seen.
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PMID:[Alpha 1-antitrypsin as an endogenous marker of protein-losing enteropathies]. 143 95

A family is described in which there occurred two cases of the lupoid type of active chronic hepatitis with cirrhosis, one of chronic persistent hepatitis, and one of myasthenia gravis. The two cases of lupoid hepatitis were in the proposita, a schoolgirl aged 16 years, and her great-aunt aged 69 years whom she had never met. The case of myasthenia gravis was that of the father. The whole family, except the great-aunt, had been exposed to an epidemic of infectious hepatitis five years previously, and the girl and her brother had contracted this disease. The schoolgirl later developed active chronic hepatitis while her brother had chronic persistent hepatitis without immunological concomitants. APART FROM COINCIDENCE, SOME COMBINATION OF THREE PROCESSES WAS REQUIRED TO ACCOUNT FOR THE ILLNESSES IN THIS FAMILY: a genetic predisposition to chronic liver disease in particular, a genetic predisposition to autoimmune reactions in general, and a ;triggering' effect of infection with the hepatitis virus.
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PMID:An interplay of genetic and environmental factors in familial hepatitis and myasthenia gravis. 548 30

An 8.5-month-old boy with Wiskott-Aldrich syndrome received a sibling matched bone marrow transplant from his healthy non-identical twin brother. The donor had primary human herpes virus 6 (HHV-6) infection around the time of bone marrow donation. The recipient had hepatitis in the first week and then developed fever and rash on day 18. Skin biopsy was shown to have HHV-6 antigen and his peripheral blood leukocytes were HHV-6 DNA positive. He engrafted on day 18 but the ANC dropped from 5.5 x 10(9)/l (day 23) to 0.48 x 10(9)/l (day 34) with persistent HHV-6 DNAemia. Bone marrow on day 35 was positive for HHV-6 DNA. He was treated with G-CSF and ganciclovir with good response. He later had pneumonitis which was treated empirically with foscarnet, ceftazidime and clarithromycin.
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PMID:Primary human herpes virus 6 infection transmitted from donor to recipient through bone marrow infusion. 963 82

Hepatitis C virus (HCV) causes non-A, non-B hepatitis and infects an estimated 170 million people worldwide. The treatment for HCV infection is often unsuccessful with high costs and many side-effects. There is a great need for alternative therapies including preventive and therapeutic vaccination for HCV infection. The experiments in this study were carried out to elucidate whether endogenously expressed antigen can be presented to helper T-cells restricted by class II molecules and to determine whether responses to plasmid-derived antigen resemble those that we have reported for recombinant antigens or synthetic peptides. To address these issues, a multi-epitope minigene was expressed in 293T-cells and Epstein-Barr virus (EBV)-transformed B-lymphoblastoid cells (BLCL). The transfected BLCLs were employed as APCs to stimulate epitope-specific T-cell hybridomas (THC). The results demonstrated that the endogenously expressed minigene antigens could be processed and presented to T-cell hybridomas by HLA matched BLCL. Five out of seven incorporated epitopes were recognized. Blockade of HLA DR could abolish the release of IL-2, which demonstrated that the endogenously expressed minigene antigens were presented by MHC class II molecules. The presentation of endogenously expressed antigens was much more efficient than that of exogenous antigens, at least in the present study. The findings obtained here have important significance for the development of an HCV DNA vaccine.
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PMID:Recognition of endogenously synthesized HLA-DR4 restricted HCV epitopes presented by autologous EBV transformed B-lymphoblastoid cell line. 1560 98

The woodchuck hepatitis virus posttranscriptional regulatory element (WPRE) is widely used in retroviral gene transfer vectors. However, this element contains an open-reading frame (ORF) encoding a truncated peptide of the woodchuck hepatitis virus X protein (WHX). Because we are developing a lentiviral vector for the gene therapy of Wiskott-Aldrich syndrome (WAS), we evaluated whether the WPRE was needed in the gene transfer cassette and tested the possibility of replacing it with a mutated derivative. The transcriptional activity of the WPRE was undetectable in the context of the lentiviral vector but the element was capable of translating a polypeptide. This capability was abrogated by mutating the WHX ORF translation start. The WPRE was required to express high levels of the transgene and for that, the native form or mutated derivatives functioned equivalently. The vector using a WAS gene promoter and the mut6 WPRE induced long-term expression of the WAS transgene in vivo, correcting cytoskeletal defects, thymocyte and B-cell numbers and improved the colitis of WAS-null mice. By providing additional evidence of efficacy of this WAS lentiviral vector with improved safety features, our results validate a mutated WPRE, which should be useful in future gene therapy applications.
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PMID:Validation of a mutated PRE sequence allowing high and sustained transgene expression while abrogating WHV-X protein synthesis: application to the gene therapy of WAS. 1926 15