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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenovirus type 5 DNA has low infectivity (Graham & van der Eb, 1973) which can be increased by various techniques, one of which is the dimethyl sulphoxide (DMSO) boost (Stow & Wilkie, 1976). In this report, it is shown that DMSO treatment of adenovirus 5 DNA-infected HeLa cells results in a 10-fold increase in plaque formation, and that this can be used to facilitate marker rescue experiments. Double DNA infections were performed by the calcium phosphate method, co-precipitating intact temperature-sensitive mutant DNA with purified wild-type DNA restriction endonuclease fragments. Analysis of the plaquing ability of these mixtures and any progeny virus has resulted in the assignment of six temperature-sensitive mutations to discrete physical locations on the adenovirus type 5 genome. These locations are discussed with respect to the mutant phenotypes and the transcription-translation products of the appropriate regions.
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PMID:Mapping of adenovirus type 5 temperature-sensitive mutations by marker rescue in enhanced double DNA infections. 74 9

Adenovirus-dependent release of choline phosphate from KB cells at pH 6.0 was partially blocked by ouabain. In K+-containing medium, maximum inhibition of release was obtained by 10(-5) M ouabain and half-maximal inhibition was achieved by about 0.5 X 10(-6)M ouabain. Ouabain did not block either the binding or the uptake of adenovirus by KB cells. Without K+, about 25% of cell-associated choline phosphate was released by adenovirus, whereas with 1 mM K+ about 50% was released. This activation by K+ was blocked by 0.1 mM ouabain. HeLa cells behaved like KB cells, but a mutant of HeLa cells resistant to ouabain (D98-OR) released much lower amounts of choline phosphate in response to human adenovirus type 2 (Ad2). Wild-type D98-OR cells bound nearly the same amount of adenovirus as did normal HeLa cells. Ad2 also increased the activity of Na+,K+-ATPase in KB cells, with maximum activation at 50 micrograms of Ad2 per ml. In D98-OR cells, Ad2 failed to activate Na+,K+-ATPase activity. Ad2-dependent lysis of endocytic vesicles (receptosomes) was assayed by measuring Ad2-dependent enhancement of epidermal growth factor-Pseudomonas exotoxin toxicity. This action of adenovirus was increased when K+ was present in the medium. Under the conditions used, K+ had no effect on the amount of Ad2 or epidermal growth factor taken up by the cells. On the basis of these results, it is suggested that Ad2-dependent cellular efflux of choline phosphate and adenovirus-dependent lysis of receptosomes may require Na+,K+-ATPase activity.
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PMID:Adenovirus-dependent changes in cell membrane permeability: role of Na+, K+-ATPase. 287 42

Chickens were experimentally infected with a duck adenovirus that has been shown to be serologically indistinguishable from Adenovirus 127. Sera and eggs were collected at intervals after exposure for antibody determination by the hemagglutination-inhibition (HI) test, the enzyme-linked immunosorbent assay (ELISA), and the immunodiffusion (ID) test. Egg yolks were processed for use in the serological tests by (a) dilution in phosphate-buffered saline (PBS), (b) extraction of the water-soluble fraction with chloroform, or (c) freezing and thawing PBS-diluted yolks and testing the supernatant fluid. HI antibody titers from serum and extracted yolk were similar except during the initial 2 weeks, when yolk antibody levels were low or absent. Chloroform-extracted yolks were suitable material for the HI, ELISA, and ID tests. Heat inactivation of the chloroform-extracted yolk had no effect on titers.
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PMID:Use of egg yolk to determine antibody levels in chickens inoculated with a hemagglutinating duck adenovirus (adenovirus 127-like). 299 38

DNA polymerase activity can be unmasked in avian myeloblastosis virus (AMV) by treatment with the nonionic detergent Nonidet P-40. Two products are formed: (1) RNA.DNA hybrid molecules and (2) duplex DNA molecules. The kinetics of dTTP incorporation into DNA are biphasic: an initial rapid reaction for 4 min at 37 degrees C with a minimal polymerization rate of 10-20 nucleotides per see, and a second reaction at about half the initial rate. Viral RNA.DNA complexes are detected as early as 30 sec after the initiation of DNA synthesis; DNA free of template is formed subsequently. Most of the free AMV DNA forms an RNA.DNA hybrid when annealed with viral RNA. Over half of the free AMV DNA product is inferred to be double-stranded, since it is retained on hydroxyapatite columns after elution with 0.12 M phosphate buffer, and is resistant to Escherichia coli exonuclease I. Adenovirus or calfthymus DNA added to unmasked AMV stimulates DNA synthesis 4-16 times if there is no treatment with RNase, and 40-130 fold if RNase treatment precedes the enzyme assay. It is possible that two polymerases are present, or that a single enzyme forms both the RNA.DNA hybrid and the double-stranded product.
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PMID:Mechanism of carcinogenesis by RNA tumor viruses. 3. Formation of RNA, DNA complex and duplex DNA molecules by the DNA polymerase (s) of avian myeloblastosis virus. 432 24

The efficiency of a system developed for the recovery of viruses contaminating large quantities of vegetables was investigated in the laboratory and tested in the field. Viruses seeded onto a number of leafy vegetables in the laboratory were eluted with a phosphate-buffered saline solution (pH 9.0). The eluate was clarified by glass wool filtration, and any viruses present were concentrated by adsorption to a Filterite pleated cartridge filter, eluted with 3% beef extract (pH 9.0), and further concentrated by organic flocculation. At least 24 liters of vegetable eluate could be concentrated to 70 to 80 ml, equivalent to a greater than 99.5% reduction in volume. With this system, poliovirus was recovered with a mean efficiency of 58% for all vegetables tested. Adenovirus was recovered from lettuce with a slightly lower mean efficiency (55%). Poliovirus was recovered from large quantities of cabbage for up to 5 days in the field after spray irrigation of relatively low levels of virus, even when heavy rain fell before sampling.
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PMID:Recovery of viruses from vegetable surfaces. 629 90

Seven viral transport media (VTM) were compared for effectiveness in preserving the infectivity of herpes simplex virus (HSV), respiratory syncytial virus (RSV), and adenovirus. The media tested were Richards viral transport, sucrose-phosphate-glutamate (SPG), Virocult, HH medium, tryptose phosphate broth, cell culture medium, and Bartel's viral transport. Two laboratory strains of HSV (McIntyre and 333) and two clinical isolates (A0301 and A0386), comprising two HSV-1 types and two HSV-2 types, were suspended in each transport medium, kept at 4 degrees C and 22 degrees C, and assayed for surviving virus at various times of up to 2 weeks. Similar testing was done with RSV Long strain and adenovirus type 2. Of the seven media, Richards viral transport, SPG, Virocult, and HH medium, followed closely by tryptose phosphate broth, best preserved HSV infectivity at both 4 degrees C and 22 degrees C. Analysis of decay rates of RSV revealed comparatively rapid decay in SPG and Virocult. Adenovirus was stable in all media and at both temperatures tested. These results indicate that viral transport and subsequent culture isolation are possible using many different VTMs if transport times are kept to a minimum (< 1 day), but if transport extends to longer times, or low levels of virus are present in the specimen, Richards viral transport and HH medium appeared to be the best overall transport media for the viruses tested.
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PMID:Comparison of various transport media for viability maintenance of herpes simplex virus, respiratory syncytial virus, and adenovirus. 782 Sep 92

Adenovirus prevents host cell protein synthesis during its late phase of replication in large part by causing the underphosphorylation of translation initiation factor eIF-4E, a component of initiation factor eIF-4F (cap-binding protein complex). Late adenovirus mRNAs are preferentially translated because they possess a reduced requirement for eIF-4F. This study continues the characterization of the mechanism by which adenovirus inhibits cellular protein synthesis. First it is shown that adenovirus blocks the addition of phosphate to eIF-4E rather than enhancing its removal, establishing that the virus impairs a signalling pathway or protein kinase activity involved in eIF-4E phosphorylation. It is then shown that shutoff of cell protein synthesis and translation of late viral mRNAs are uncoupled, in that shutoff actually occurs a short time (1 to 3 h) after late adenovirus mRNAs are already undergoing translation. Finally, by using a variety of genetic mutants stalled at different stages in the viral life cycle, it was found that dephosphorylation of eIF-4E and inhibition of cell translation are not caused by early adenovirus gene products acting at late times or by events related to viral DNA replication. Instead, it is shown that inhibition of eIF-4E phosphorylation and cell translation are mediated upon activation of the viral major late transcription unit. These and other results presented indicate that the adenovirus signal which induces eIF-4E dephosphorylation and shutoff of cell protein synthesis is linked either to an activity of one or more late viral polypeptides, to double-stranded RNA produced by opposition of the early and late viral transcription units, or to both.
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PMID:A late adenovirus factor induces eIF-4E dephosphorylation and inhibition of cell protein synthesis. 793 86

Studies of the regulation of androgen synthesis in steroidogenic cells have focused on both transcriptional and post-translational regulation of the proteins that catalyze these reactions: the P450c17 that catalyzes the production of DHEA or androstenedione in consecutive hydroxylase and lyase activities, and the 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) that catalyzes the conversion of androstenedione to testosterone. Our studies of the regulation of the CYP17 lyase activity at the molecular level have utilized species- and tissue-specific differences to identify target regulatory sequences. Adenovirus infection of rat CYP17 promoter/luciferase reporter gene constructs in primary cultures of rat adrenal and rat Leydig cells revealed a rat-specific domain between-1 and -108 bp that cause inhibition of both basal and cAMP-induced CYP17 transcription in the adrenal, but not the Leydig cell. In contrast, similar promoter constructs from other species exhibited substantial cAMP-induced transcriptional activity in the rat adrenal. Mutagenesis of the conserved region of the rat and human proteins reveals significant differences in the amino acid domains required for hydroxylase and lyase activities within and between the two species, consistent with their differential regulation of lyase activity. The 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) reaction requires a viable glucose transporter system for optimal activity, and a high-energy phosphate was discovered to be the requisite product of glucose metabolism in 17 beta-HSD activation. These studies have provided insight into potential mechanisms of control of androgen synthesis in the late steroidogenic pathway, at the transcriptional and post-translational levels.
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PMID:Regulation of androgen synthesis: the late steroidogenic pathway. 902 27

An apparently novel adenovirus was associated with an epizootic of hemorrhagic disease that is believed to have killed thousands of mule deer (Odocoileus hemionus) in California (USA) during 1993-1994. A systemic vasculitis with pulmonary edema and hemorrhagic enteropathy or a localized vasculitis associated with necrotizing stomatitis/pharyngitis/glossitis or osteomyelitis of the jaw were common necropsy findings in animals that died during this epizootic. Six black-tailed yearling deer (O. hemionus columbianus) were inoculated with purified adenovirus isolated from a black-tailed fawn that died of acute adenovirus hemorrhagic disease during the epizootic. Three of six inoculated deer also received intramuscular injections of dexamethasone sodium phosphate every 3 days during the study. Eight days post-inoculation, one deer (without dexamethasone) developed bloody diarrhea and died. Necropsy and histopathologic findings were identical to lesions in free-ranging animals that died of the natural disease. Hemorrhagic enteropathy and pulmonary edema were the significant necropsy findings and there was microscopic vascular damage and endothelial intranuclear inclusion bodies in the vessels of the intestines and lungs. Adenovirus was identified in necrotic endothelial cells in the lungs by fluorescent antibody staining, immunohistochemistry and by transmission electron microscopy. Adenovirus was reisolated from tissues of the animal that died of experimental adenovirus hemorrhagic disease. Similar gross and microscopic lesions were absent in four of six adenovirus-inoculated deer and in the negative control animal which were necropsied at variable intervals during the 14 wk study. One deer was inoculated with purified adenovirus a second time, 12 wk after the first inoculation. Fifteen days after the second inoculation, this deer developed severe ulceration of the tongue, pharynx and rumen and necrotizing osteomyelitis of the mandible which was associated with vasculitis and thrombosis of adjacent large vessels and endothelial intranuclear inclusions. Transmission electron microscopy demonstrated adenovirus within the nuclei of vascular cells and immunohistochemistry demonstrated adenovirus antigen within tonsilar epithelium and in rare vessels.
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PMID:Experimental adenovirus hemorrhagic disease in yearling black-tailed deer. 939 65

Adenovirus-mediated overexpression of the glucose phosphorylating enzyme glucokinase causes large changes in glycolytic flux and glucose storage in isolated rat hepatocytes, but not in pancreatic islets. We have used the well-differentiated insulinoma cell line INS-1 to investigate the basis for these apparent cell-type specific differences. We find that 2- or 5-[3H]glucose usage is increased at low (</=5 mM) but not high glucose concentrations in INS-1 cells treated with a recombinant adenovirus containing the glucokinase cDNA (AdCMV-GKI), while glucose usage is increased at both low and high glucose concentrations in similarly treated hepatocytes. Utilization of 2-[3H]glucose in INS-1 cells is suppressed in glucokinase overexpressing INS-1 cells in a rapid, glucose concentration-dependent, and reversible fashion, while such regulation is largely absent in hepatocytes. Levels of hexose phosphates (glucose-6-phosphate, fructose-6-phosphate, and fructose-1,6-bisphosphate) were profoundly and rapidly elevated following the switch to high glucose in either AdCMV-GKI-treated INS-1 cells or hepatocytes relative to controls. In contrast, triose phosphate levels (glyceraldehyde-3-phosphate + dihydroxyacetone phosphate) were much higher in AdCMV-GKI-treated INS-1 cells than in similarly treated hepatocytes, suggesting limited flux throught the glyceraldehyde-3-phosphate dehydrogenase (G3PDH) step in the former cells. Hepatocytes were found to contain approximately 62 times more lactate dehydrogenase (LDH) activity than INS-1 cells, and this was reflected in a 3-fold increase in lactate production in AdCMV-GKI-treated hepatocytes relative to similarly treated INS-1 cells. Since the amounts of G3PDH activity in INS-1 and hepatocyte extracts are similar, we suggest that flux through this step in INS-1 cells is limited by failure to regenerate NAD in the LDH reaction and that a fundamental difference between hepatocytes and islet beta-cells is the limited capacity of the latter to metabolize glycolytic intermediates beyond the G3PDH step.
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PMID:Fundamental metabolic differences between hepatocytes and islet beta-cells revealed by glucokinase overexpression. 952 75


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