Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electron and immunoelectron microscopic studies were carried out on liver tissues from three marmosets, experimentally infected with hepatitis A virus and sacrificed during the acute phase of illness. Ultrastructurally, the liver cells demonstrated marked cisternal dilation of endoplasmic reticulum and vesicular transformation and contortion of endoplasmic reticulum profiles. Clusters of virus-like particles of 24 to 27 nm. in diameter, both "solid" and "empty" forms, were found in membrane-bound cytoplasmic vesicles. In one animal, the virus-like particles were significantly smaller, measuring 17 to 22 nm. in size, and almost all were solid forms embedded in an amorphous matrix. Clusters of virus-like particles were found in the bile canaliculi of liver cell cords and in lysosomal structures of monocytes or Kupffer cells in the hepatic sinusoids. The latter correlated with the immunofluorescent microscopic finding. Indirect immunoferritin staining was carried out on fresh and formalin-fixed liver tissues, using convalescent phase serum from patients recovered from hepatitis A virus infection as the primary antibody, and the ferritin-labeled rabbit anti-human IgG or ferritin-labeled staphylococcal protein A as the secondary antibody. Specific stainings were observed with the virus-like particles, indicating that the particles were probably antigenically related to hepatitis A virus. Our findings are in agreement with the immunofluorescent and immunoelectron microscopic studies reported by others and support the concept that hepatitis A virus is produced in the liver. The infection seems to produce cytopathic effect especially to the endoplasmic reticulum organelle of hepatocytes.
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PMID:Electron and immunoelectron microscopic study on liver tissues of marmosets infected with hepatitis A virus. 22 41

We evaluated the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in 78 Italian patients with hereditary hemochromatosis as well as the relation between HCV antibody (anti-HCV) status, hepatitis B surface antigen (HBsAg) and liver histology. None of the patients had been transfused or ever consumed more than 60 g of alcohol per day. Eighteen showed histological signs of chronic hepatitis, active cirrhosis was present in 12, chronic active hepatitis in 4 and chronic persistent hepatitis in 2. Liver fibrosis or cirrhosis without inflammatory activity was observed in 31 subjects, whereas liver histology was normal except for iron overload in 18. The prevalence of HBsAg in the whole series was 5% and of anti-HCV was 20.5%. The prevalence of HBsAg and anti-HCV was significantly higher in the chronic hepatitis group than in the fibrosis/cirrhosis (p = 0.01) and the normal groups (p < 0.01). Fourteen of 18 hereditary hemochromatosis patients with chronic hepatitis were HBsAg (4) or anti-HCV (10) positive and all the latter subgroup had HCV-RNA in their serum as shown by the polymerase chain reaction. Although most of the patients with associated chronic hepatitis had cirrhosis, their serum ferritin levels and amount of mobilizable iron were significantly lower than those of the fibrosis/cirrhosis group (p < 0.01). This indicates that hepatitis viral infection acts synergistically with iron in accelerating the development of liver damage.
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PMID:Liver damage in Italian patients with hereditary hemochromatosis is highly influenced by hepatitis B and C virus infection. 148 15

A human hepatocellular carcinoma cell line, JHH-7, was established from resected liver tumor of a 53 year old male with hepatitis B virus infection. JHH-7 was composed of polygonal epithelial cells and functionally synthesized and secreted human albumin, AFP, CEA and ferritin. No HBsAg was detected in the culture supernatant of JHH-7 cells. Changes of secretion of AFP and CEA from JHH-7 cells after heat treatment was studied using a temperature gradient incubator. Secretion of AFP decreased along with the inhibition of cell proliferation by heat treatment. Secretion of CEA, however, did not decrease even though the cells were damaged.
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PMID:[Establishment and characterization of a human hepatocellular carcinoma cell line JHH-7 producing alpha -fetoprotein and carcinoembryonic antigen--changes in secretion of AFP and CEA from JHH-7 cells after heat treatment]. 170 54

To define the hematologic changes during a mild viral infection, 93 infants were immunized with live attenuated measles virus and studied prospectively at 0, 4, 9, 14, 21, and 30 days. Hemoglobin concentration decreased significantly by days 9 and 14. The decrease was greater than 1.0 g/dL in 8.6% and greater than 0.6 in 24.3% of the infants. Of the nonanemic infants, 22% became anemic. Serum iron and percentage saturation of transferrin decreased, whereas serum ferritin increased significantly. Mean cell volume, iron-binding capacity, protoporphyrin, and haptoglobin did not show changes. Reticulocyte index and erythropoietin increased significantly at 30 days. Leukocyte counts, Zetacrit, and C-reactive protein did not help to predict the hemoglobin decrease. These results suggest that a mild viral infection in infants induces a significant decrease in hemoglobin that may persist for 14 to 30 days and may be difficult to distinguish from iron deficiency.
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PMID:Anemia of a mild viral infection: the measles vaccine as a model. 279 79

Higher serum iron and ferritin levels noted in hepatitis B antigen (HBAg) carriers than in noncarriers suggests that virus might actively replicate in hepatocytes, stimulate ferritin synthesis, and result in increased liver iron stores. A comparative semiquantitative study of immunohistochemical ferritin (0-12) and hemosiderin (0-9) was performed on 54 normal, 13 cirrhotic, and 70 nonneoplastic livers from patients with hepatocellular carcinoma, in each group, comparing amounts in HBAg-positive and HBAg-negative patients. Mean scores for ferritin and hemosiderin were high in all three groups, normal livers averaging 8.3 and 6, respectively, cirrhotic livers, 8.5 and 7.4, respectively, and carcinoma livers, 5.6 and 6.1, respectively. In each group, there was no significant difference in ferritin and hemosiderin mean scores in HBAg-positive and HBAg-negative patients. The large liver iron stores do not appear to be a consequence of hepatitis B virus infection alone. Their role in the development of hepatocellular carcinoma is still to be elucidated.
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PMID:Liver iron stores and hepatitis B antigen status. 299 50

With hemodialysis patients, a high serum ferritin before there was serological evidence of hepatitis B virus infection increased the likelihood that the infection would be persistent. This finding suggested that hepatitis B virus is likely to infect and actively replicate in liver cells with the propensity for increased ferritin synthesis. The virus itself could stimulate the synthesis of ferritin in a cyclic positive feedback mechanism that increases intracellular ferritin concentration and, eventually, intracellular iron. Transformed liver cells have low iron content, do not replicate hepatitis B virus, and require iron for growth. Infected, nonmalignant liver cells could supply iron to the transformed cells and nourish their expansion.
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PMID:Serum ferritin as a predictor of host response to hepatitis B virus infection. 630 Oct 8

Neurologic diseases are important complications of measles. The role of virus infection of the central nervous system as well as the route of virus entry has been unclear. Five autopsied cases of individuals who died with severe acute measles 3-10 d after the onset of the rash were studied for evidence of viral involvement of the central nervous system. In all cases, in situ hybridization and RT-PCR in situ hybridization techniques showed endothelial cell infection. Immunoperoxidase staining with an anti-ferritin antibody revealed a reactive microgliosis. These data suggest that endothelial cells in the brain are frequently infected during acute fatal measles. This site of infection may provide a portal of entry for virus in individuals who subsequently develop subacute sclerosing panencephalitis or measles inclusion body encephalitis and a target for immunologic reactions in post-measles encephalomyelitis.
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PMID:Brain endothelial cell infection in children with acute fatal measles. 759 37

Chronic hepatitis C has been demonstrated to be associated with hepatic iron overload, and the hypothesis that the disease activity of hepatitis C is associated with iron cytotoxicity was tested in male volunteer blood donors. Sera with either antibody to hepatitis C virus or hepatitis B surface antigen were selected for determination of ferritin concentration and alanine aminotransferase activity. A correlation between serum ferritin concentration (Y; microgram/l) and alanine aminotransferase activity (X; IU/l) was found in donors with antibody to hepatitis C (log Y = 0.65 x log X + 0.98, r = 0.53, and P < 0.01). The correlation was lower in donors with hepatitis B surface antigen (r = 0.37; P < 0.01). Hepatitis C virus infection probably induces time-dependent iron accumulation associated with the progression of disease activity, while hepatitis B virus infection results in a variety of iron loads with different clinical features. The high disease activity related to hyperferritinemia suggests the presence of iron-induced liver damage in donors with hepatitis C.
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PMID:Correlation between serum levels of alanine aminotransferase and ferritin in male blood donors with antibody to hepatitis C virus. 800 May 7

Twenty-seven children with mumps or chickenpox were taken as a model to evaluate the haematological consequences of viral infections including serum iron status. Blood samples were obtained from all patients at presentation and on the 21st day of the disease. While haemoglobin, haematocrit, and mean corpuscular volume levels were similar in two measurements (P > 0.05), the mean leucocyte, absolute lymphocyte and thrombocyte counts, mean serum iron, serum iron binding capacity and transferrin saturation levels were lower at presentation than on the 21st day of the disease. The serum iron levels were below 30 micrograms/dl in 16 (59.2%) patients at presentation while only 4 (14.8%) had low values on 21st day. Twenty-four (88.9%) patients had an increment in the serum iron binding capacity levels and 2 (7.6%) reached values above the normal range on the 21st day. In 21 (77.8%) patients, the transferrin saturation levels were below the expected ranges at presentation but 26 (96.3%) showed an increment on the 21st day. However, the mean ferritin level was higher at presentation. Therefore, during the evaluation of patients for anaemia, the presence of a recent acute viral infection should be documented so as to avoid unnecessary iron medication.
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PMID:Haematologic consequences of viral infections including serum iron status. 818 99

Mengo virus infection of mouse L-cells results in induction of the synthesis of a cellular protein-containing particle, 12 nm in diameter, which was designated U (Boege et al. (1987) Virology 159, 358-367). We have purified the U-particle from virus-infected cells by a series of chromatographic steps and found it to be composed of two polypeptide species (MW 23,000 and 25,000), present in a ratio of approximately 7:3. Neither of these polypeptides is measurably glycosylated or phosphorylated and the U-particle contains no detectable nucleic acid. Several amino acid sequences obtained from CNBr fragments of the U-polypeptides identified them as the H- and L-chains of mouse apoferritin. This finding was supported by immunoblotting and electron microscopy. In terms of function, the U-particle/apoferritin effectively inhibits the translation of mRNAs in reticulocyte lysates. These experiments indicate that apoferritin may perform important functions in eukaryotic cells in addition to iron storage. Finally, we propose mechanisms to explain how Mengo virus infection could specifically induce the synthesis of apoferritin and how increasing amounts of cytoplasmic apoferritin could facilitate virus replication.
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PMID:The cellular U-particle, whose synthesis is induced by mengovirus infection, is homologous to apoferritin. 825 85


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