Budesonide-induced acute hepatitis in an HIV-positive patient with ritonavir as a co-medication.
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Acute Disease↗
Biomedical subjects
Andreas Erhardt
Publications and source records attributed to Andreas Erhardt.
A seropneumothorax?
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Diagnosis, Differential↗
Hepatitis C virus core protein induces cell proliferation and activates ERK, JNK, and p38 MAP kinases together with the MAP kinase phosphatase MKP-1 in a HepG2 Tet-Off cell line.
Hepatitis C virus (HCV) core protein is a multifunctional protein interacting with cellular and viral proteins and promoters. A tetracycline-regulated system was used to generate a HepG2 Tet-Off cell line allowing regulated expression of a full-length (191 aa) and an N(c)-truncated core protein (160 aa). In this system HCV core protein expression activates extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 mitogen-activated protein (MAP) kinase, induces MAP kinase phosphatase MKP-1 expression, and increases cell proliferation. This was accompanied by an activation of c-Jun and ATF-2, but not Elk-1 and c-Fos. Furthermore, AP-1 activation was independent of c-Fos. Full-length and N(c)-truncated HCV core proteins exerted similar effects.
Cell Line↗
Cloning and molecular characterization of human high affinity antibody fragments against Hepatitis C virus NS3 helicase.
Hepatitis C Virus (HCV) non-structural protein 3 (NS3) helicase is essential for viral replication. Cloning of human antibody fragments for binding and inhibiting HCV helicase intracellularly (intracellular immunization) was attempted. A phage display system was employed to isolate human sFv fragments. A large phagemid library was cloned from patients infected with HCV. Phages expressing human sFv fragments with binding activity against NS3 were highly enriched during affinity selection. Selected sFv antibody fragments showed high affinity to HCV helicase. The variable domains of the cloned antibody fragments were sequenced and their germ-line origin was determined. K(D) values describing affinity of sFv to NS3 were measured by competition-EIA. Bacterially expressed recombinant human high affinity antibodies can be used for diagnostic and therapeutic purposes. Further experiments will select antibody fragments inhibiting NS3 helicase. Employing vectors for transduction of the encoding cDNA into infected cells might be a novel gene therapy strategy for intracellular immunization against chronic HCV infection.
Amino Acid Sequence↗
HFE gene mutations and iron metabolism in Wilson's disease.
BACKGROUND: There is increasing evidence for an interaction between iron and copper metabolism. METHODS: Iron indices (ferritin, transferrin saturation [TS], serum iron), liver parameters, the prevalence and significance of C282Y and H63D HFE mutations were studied in 40 unrelated, Caucasian patients with Wilson's disease and 295 healthy controls. Due to specific treatment Wilson's disease was well controlled in all but one patient. RESULTS: The allele frequencies for the C282Y (11.3% vs. 6.2%) and the H63D (18.8% vs. 16.4%) mutation did not differ between patients with Wilson's disease and healthy controls. One patient with C282Y homozygous HH and Wilson's disease was identified showing progressive liver disease despite reasonable venesection and copper chelation therapy. No differences in iron indices and liver values were seen between HFE heterozygous and HFE wildtype patients with Wilson's disease. Higher serum ferritin levels were noticed in patients with Wilson's disease compared to healthy controls (149 +/- 26 microg/l vs. 87 +/- 8 microg/l; P < 0.03). CONCLUSIONS: It appears reasonable to assess iron indices in patients with Wilson's disease in order to detect iron overload. HFE mutations other than C282Y homozygosity seem to have no impact on iron indices and liver parameters as long as Wilson's disease is controlled.
Adolescent↗
SEN virus infection.
The SEN virus (SEN-V) belongs to a recently discovered group of DNA viruses whose members (SEN-V-D and SEN-V-H) are associated with post-transfusion hepatitis. It is a single-stranded circular, non-enveloped DNA virus of approximately 3600 to approximately 3800 nucleotides with at least three open reading frames (ORFs). Eight different strains of SEN-V have been identified and provisionally classified as members of the Circoviridae family, a group of small, single-stranded, non-enveloped circular DNA viruses that includes the TT virus (TTV), TUS01, SANBAN, PMV and YONBAN. Prevalences in different populations show great variability with marked differences between different countries and groups. Although parenteral transmission is very likely, other routes of transmission cannot be excluded. Mother to infant transmission has been demonstrated. The effect of SEN-V on chronic liver diseases has been studied. The influence of SEN-V on the response to HCV therapy was investigated in three studies, with contradictory results. Data for other acute and chronic liver diseases are sparse. Further studies are needed to define the pathogenesis and clinical importance of SEN-V infection.
Adult↗