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)

Human serum having complement fixation anti-herpex simplex virus activity was reacted with herpes simplex virus infected cells in tissue culture. By tagging the antibody to ferritin and examining the cells in the electron microscope, it was found that 1. the entire surface of the infected cell is antigenically altered and reacts with hyperimmune serum. The antigenic cell surface change is not limited to structurally altered sites, nor is it limited to sites where virus particles are present, and 2. cells in the early stages of infection react more strongly with hyperimmune serum than do cells in later stages. The possible clinical significance of the infected cell surface - antibody reaction is discussed.
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PMID:Altered immunologic specificity of cells infected with Herpes simplex virus: recognition of human antiserum. 17 Jul 50

Using ferritin as a marker of reactive microglia, we demonstrated a close association between proliferation of reactive microglia and expression of human immunodeficiency virus type 1 (HIV-1) in brain tissue from autopsied cases of acquired immunodeficiency syndrome (AIDS). An increased number of ferritin-positive reactive microglia was observed in formalin-fixed paraffin-embedded brain sections from all 13 AIDS cases examined. Similar findings were observed in brain tissue from other neurological diseases (subacute sclerosing panencephalitis, herpes simplex encephalitis and multiple sclerosis). Multinucleated giant cells were found in 7 of the AIDS cases which were also intensely labeled for ferritin. Dual-label immunohistochemistry using anti-ferritin and cell-specific markers showed that ferritin-positive cells were distinct from astrocytes, neurons and endothelia using anti-glial fibrillary acidic protein (anti-GFAP), anti-neurofilament protein and Ulex europaeus agglutinin 1, respectively. In 5 AIDS brains, only ferritin-positive cells were shown to contain HIV-1 gp41 antigen using dual-label immunohistochemistry. In addition, HIV-1 RNA was localized in ferritin-positive reactive microglia but not in GFAP-positive astrocytes using immunohistochemistry combined with in situ hybridization. Ferritin-positive reactive microglia and multinucleated giant cells were co-labeled with the microglial marker, Ricinus communis agglutinin 1 (RCA-1). However, RCA-1 also extensively stained resting microglia only a few of which were co-labeled for ferritin. The density of ferritin-positive cells was correlated with the presence of HIV-1 RNA-positive cells in AIDS brain. Thus, ferritin immunoreactivity can be used as an activation marker of microglia in archival paraffin sections and reflects the extent of inflammation in HIV-1-infected brain.
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PMID:Simultaneous detection of ferritin and HIV-1 in reactive microglia. 141 82

The process of fusion from without (FFWO) induced by herpes simplex virus (HSV) was analyzed by using various inhibitors and compared to fusion from within (FFWI). The fate of certain elements of the cytoskeleton after FFWO was also investigated. Our experiments demonstrate FFWO as a very suitable system for study of early virus-cell interactions. Zn++ ions proved inhibitory for penetration whilst pretreatment of cells with Ca++ ions before infection enhanced FFWO activity. Dissociation of penetration from the fusion process itself was possible by use of Zn++ ions, low pH-treatment and antiserum on the one hand and N-ethylmaleimide and cytochalasin D on the other. Penetration itself needs only 6 min or less to proceed. FFWO is independent of inhibitors of glycosylation (tunicamycin) and intracellular vesicular traffic (monensin), protein-synthesis (cycloheximide) and energy-delivery (2.4 dinitrophenol and Na-azide). Analyzed strains of HSV-1 and -2 producing FFWI could be subgrouped into three categories: Strain ANG with high, strain HFEM and Lux with low and strains IES, Len, MP, US with no FFWO activity. The results of these experiments indicate that the property of FFWO is not purely a consequence of the number of PFU but depends on certain inherent properties of the virus particles. Addition of heparin as well as treatment of cells with heparitinase effectively prevented FFWO, indicating identical virus receptors for entrance of virus into cells and FFWO. During our studies several calf sera were found to inhibit FFWO-activity. Inhibition of FFWO by a glycoconjugate (ferritin coupled with oleic acid) indicates specific stereochemical hindrance of FFWO by this compound. Shortly after FFWO the actin filaments rearrange to form long fibres and surface fibronectin is being lost from the cell membrane.
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PMID:Characterization of fusion from without induced by herpes simplex virus. 184 50

We have previously purified an Mr 75,000 protein from cultured human JEG-3 choriocarcinoma cells and showed that this protein is specifically confined to the cytoplasmic side of JEG-3 microvillar membranes. Recently, the Mr 75,000 protein, designated as cytovillin, was found to be expressed also in several other cultured human cell lines and strains, in which it was detected in microvillus-related structures. We now demonstrate the redistribution of cytovillin in herpes simplex type 1 (HSV-1) and Semliki Forest virus (SFV) infected human embryonal fibroblasts. Virus infection induced rapidly numerous microvilli on the apical cell surfaces, and cytovillin was enriched into these newly formed structures as shown by indirect immunofluorescence and immunoferritin electron microscopy. In mock-infected cells treated with the anti-cytovillin antibodies a small amount of ferritin particles and faint fluorescence was detected along the smooth plasma membrane. Only occasional cell surface protrusions were observed in these cells. The enrichment of the cytovillin was first seen 2 h after infection. The isoelectric point (IP) and the mobility of the cytovillin polypeptide in sodium dodecyl sulfate polyacrylamide gel electrophoresis was not altered after this redistribution, suggesting that the protein was not significantly modified during infection. Five RNA+ SFV mutants (ts-1, ts-2, ts-3, ts-5, ts-7) with temperature-sensitive defects in processing and transport of viral envelope glycoproteins to the plasma membrane induced microvilli at the restrictive temperature (39 degrees C) as the wild type virus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Redistribution of Mr 75,000 plasma membrane protein, cytovillin, into newly formed microvilli in herpes simplex and Semliki Forest virus infected human embryonal fibroblasts. 284 3

We used wide-field specular microscopy to examine 60 eyes with clinically evident corneal epithelial abnormalities in vivo. The progression of epithelial edema from early basal edema to later bullous changes and eventual subepithelial fibrovascular ingrowth was observed in 35 eyes. Three eyes with filamentary keratitis displayed a protruding mucoid filament or actual mucus incorporation into the epithelium with surrounding distortion of superficial cells. Abnormally shaped and interdigitated epithelial cells were present as a result of trophic ulceration caused by herpes simplex keratitis. The Fleischer ring of ferritin deposits. Surface epithelial cells in this disorder were elongated and contained increased numbers of dark cells in more severe cases. The raised granular lesion of Thygeson's superficial punctate keratitis and subepithelial deposits in cases of basement membrane dystrophy were also observed. Invading fibrovascular tissue was identified in superficial pannus.
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PMID:In vivo microscopic observations of human corneal epithelial abnormalities. 706 95

Regulation of circulating iron is important in bacterial, yeast, and fungal infections. In the present study, cerebrospinal fluid levels of ferritin, an iron-binding protein, were determined in controls and in patients with central nervous system pyogenic and viral infections. Among 441 controls, cerebrospinal fluid ferritin level was higher than 18 ng/mL in two relapsed patients with central nervous system leukemia, 12 with bacteremia or pneumonia, and one with hemorrhagic herpes simplex encephalitis. Cerebrospinal fluid ferritin levels were more than 18 ng/mL in 13 of 63 patients diagnosed with nonhemorrhagic aseptic meningitis/ventriculitis, when defined solely by negative cerebrospinal fluid culture. Conversely, cerebrospinal fluid ferritin exceeded 18 ng/mL in culture-proven meningitis (46 of 47 cases) and ventriculitis (five of five cases). Cases of indolent cryptococcus and tuberculous meningitis showed modest increases despite traditional cerebrospinal fluid markers, at times, being normal. Cerebrospinal fluid ferritin levels did not correlate with cerebrospinal fluid neutrophil count, cerebrospinal fluid protein concentration, serum ferritin level, or patient age. In 16 of 19 cases monitored sequentially during ongoing antibiotic treatment, levels remained over 18 ng/mL (average, 15.0 days; range, 1 to 54 days). This observation suggests that obtaining cerebrospinal fluid ferritin levels is helpful whenever traditional laboratory benchmarks normalize, as during acute or chronic antibiotic therapy, or create confusion with positive cultures stemming from sample contamination.
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PMID:A persistent biochemical marker for partially treated meningitis/ventriculitis. 778 15

The efficient replication of large DNA viruses requires dNTPs supplied by a viral ribonucleotide reductase. Viral ribonucleotide reductase is an early gene product of both vaccinia and herpes simplex virus. For productive infection, the apoprotein must scavenge iron from the endogenous, labile iron pool(s). The membrane-permeant, intracellular Fe(2+) chelator, 2,2'-bipyridine (bipyridyl, BIP), is known to sequester iron from this pool. We show here that BIP strongly inhibits the replication of both vaccinia and herpes simplex virus, type 1. In a standard plaque assay, 50 microm BIP caused a 50% reduction in plaque-forming units with either virus. Strong inhibition was observed only when BIP was added within 3 h post-infection. This time dependence was observed also in regards to inhibition of viral late protein and DNA synthesis by BIP. BIP did not inhibit the activity of vaccinia ribonucleotide reductase (RR), its synthesis, nor its stability indicating that BIP blocked the activation of the apoprotein. In parallel with its inhibition of vaccinia RR activation, BIP treatment increased the RNA binding activity of the endogenous iron-response protein, IRP1, by 1.9-fold. The data indicate that the diiron prosthetic group in vaccinia RR is assembled from iron taken from the BIP-accessible, labile iron pool that is sampled also by ferritin and the iron-regulated protein found in the cytosol of mammalian cells.
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PMID:Intracellular chelation of iron by bipyridyl inhibits DNA virus replication: ribonucleotide reductase maturation as a probe of intracellular iron pools. 1130 21

A 26-year-old woman presented with general fatigue, persistent fever, nuchal lymphadenitis, thrombocytopenia, and liver damage. From the bone marrow finding, we diagnosed her condition as hemophagocytic syndrome. Steroid pulse therapy, cyclosporin A treatment, and combined chemotherapy generated no response. The patient showed severe mucosal bleeding, rapidly experienced multiple organ failure, and finally died of a brain hemorrhage on the 13th hospital day. Epstein-Barr virus, cytomegalovirus, human herpes virus type 6, human parvovirus B19, and herpes simplex virus were not detected. Autopsied samples of the spleen, bone marrow, and liver showed extreme proliferation of activated macrophages, so-called histiocytes, without lymphoid malignancy. The interferon gamma level at presentation was prominently high. The continuously elevated levels of ferritin and soluble interleukin 2 receptor were correlated with the catastrophic outcome. The disease in our case mimicked infantile hemophagocytic lymphohistiocytosis. However, there was neither a family history of the disease nor a mutation in the perforin gene. So, it is reasonable to categorize our case as macrophage activation syndrome. Although our patient lacked arthritis or eruption, we cannot deny the possibility that an oligoarthritis type of systemic-onset juvenile rheumatoid arthritis or, considering the patient's age, adult-onset Still disease lies at the base of our case.
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PMID:Fulminant hemophagocytic syndrome with a high interferon gamma level diagnosed as macrophage activation syndrome. 1523 1

Neonatal disseminated herpes simplex virus (HSV) infection with acute liver failure (ALF) and neonatal hemophagocytic lymphohistiocytosis (HLH) are severe diseases. We recently experienced a male infant with HLH and ALF induced by HSV type 1 (HSV-1). The infant, born at 39 weeks of gestation by normal delivery, developed a fever on day 4. On day 9, laboratory investigations showed progressive liver dysfunction and coagulopathy, and the serum ferritin was excessively elevated. Furthermore, the blood levels of interleukin (IL)-6, IL-10, and interferon-gamma were also elevated. HSV-1 DNA was detected in the serum and cerebrospinal fluid by the real-time PCR method. A diagnosis of HLH was established based upon the following criteria: fever, splenomegaly, cytopenia (two cell lines), serum ferritin (> 500 mug/l) and hypofibrinogenemia (< 150 mg/dl). High-dose acyclovir therapy, steroid pulse therapy using methylprednisolone, high-dose gamma globulin therapy and a blood transfusion were given. The patient recovered without neurological deficit. Neonatal disseminated HSV infections may be complicated by the development of HLH and hypercyokinemia. If HLH is suspected, not only high-dose acyclovir therapy but also anti-cytokine therapy should be considered.
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PMID:Successful treatment of neonatal herpes simplex-type 1 infection complicated by hemophagocytic lymphohistiocytosis and acute liver failure. 1821 81

A 14-day-old neonate was transferred to our university hospital because of respiratory distress and mild disturbance of consciousness. He had no history of abnormal pregnancy or delivery, but had developed apnea at 6 days old. Thereafter, respiratory distress progressed and his condition deteriorated. On admission to our hospital, several vesicles were found on the left upper arm, and moderate hepatomegaly was also present. Herpes simplex virus (HSV) type II genome was detected from serum, spinal fluid, and bone marrow. Laboratory examinations revealed typical abnormalities of disseminated intravascular coagulation, increased levels of serum ferritin, aspartate aminotransferase, and lactate dehydrogenase. Bone marrow aspiration demonstrated activated macrophages and hemophagocytosis. Spinal tap revealed numerous mononuclear cells. Meningitis and virus-associated hemophagocytic syndrome (VAHS) due to systemic HSV type II infection were thus diagnosed. Acyclovir (60 mg/kg/day) and vidarabine were promptly administered. Dexamethasone palmitate and intravenous cyclosporine were also administered for systemic inflammation due to VAHS. Finally, these aggressive therapies rescued the patient without any sequelae. In general, neonatal systemic HSV infection is life-threatening and results in poor intact survival. Our case report suggests that not only antiviral treatment for HSV, but also anti-inflammatory treatment including steroid and cyclosporine should be considered from the early phase of neonatal systemic HSV infection.
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PMID:[Neonatal herpes simplex type II virus infection complicated with meningitis and virus-associated hemophagocytic syndrome]. 2237 49


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