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D H Harter

Publications and source records attributed to D H Harter.

68 records · Page 4Linked to original sources
PubMed1967

Studies on pneumonia virus of mice (PVM) in cell culture. I. Replication in baby hamster kidney cells and properties of the virus.

Pneumonia virus of mice (PVM) has been serially propagated in a line of baby hamster kidney (BHK21) cells. A maximum titer of 6.3 x 10(6) TCID(50) per ml was obtained, and there was little variation in yield on serial passage. PVM grown in BHK21 cells was antigenically similar to virus obtained from the mouse lung, but was somewhat less virulent for the mouse after 10 serial passages in these cells. Virus produced by BHK21 cells agglutinated mouse erythrocytes without prior heating or other treatment. Sedimentation of PVM in the ultracentrifuge or precipitation by ammonium sulfate resulted in a loss in infectivity but an increase in hemagglutinating activity, presumably due to disruption of the virus particle. In a potassium tartrate density gradient, the major portion of infective virus sedimented at a density of approximately 1.15, and noninfective hemagglutinin, at a density of approximately 1.13. Stock virus preparations appear to contain a large amount of noninfective hemagglutinin. The replication of PVM was not inhibited by 5-fluoro-2'-deoxyuridine, 5-bromo-2'-deoxyuridine, or 5-iodo-2'-deoxyuridine. Infected cells contained eosinophilic cytoplasmic inclusions which showed the acridine orange staining characteristic of single-stranded RNA. Foci of viral antigen were observed in the cytoplasm of infected cells by fluorescent antibody staining. The results suggest that PVM is an RNA virus that replicates in the cytoplasm.

Animals↗
PubMed1967

Studies on pneumonia virus of mice (PVM) in cell culture. II. Structure and morphogenesis of the virus particle.

Pneumonia virus of mice (PVM) particles are spheres 80-120 mmicro in diameter, or filaments of similar diameter with lengths up to 3 micro. The particles possess an outer spike-covered envelope and helical internal component 120-150 A in diameter. Virus particles acquire their envelope by a budding process at the cell membrane; mature particles are seen only extracellularly. Dense inclusions are prominent in the cytoplasm of PVM-infected BHK21 cells by 48 hr after inoculation. The inclusions appear to consist of aggregates of the internal component of PVM, and the helical component has been isolated in a cesium chloride gradient from extracts of osmotically shocked cells. Murine erythrocytes, which are agglutinated by PVM, adsorb to the surface of infected cells and to budding and extracellular PVM particles. On the basis of its structure and morphogenesis, PVM appears to be a myxovirus; however, it does not fit into either of the established subgroups of myxoviruses. The 120-150 A diameter of the PVM internal component differs from the diameters of the internal components of the two established subgroups of myxoviruses, and suggests that a third subgroup of these viruses may exist.

Adsorption↗
PubMed1967

Immunofluorescence and cytochemical studies of visna virus in cell culture.

Sequential morphological changes occurring in sheep choroid plexus cells infected with visna virus were studied by direct immunofluorescence, acridine orange, and hematoxylin and eosin staining methods. Specific immunofluorescence was first detected in the perinuclear cytoplasm of solitary cells 24 hr after infection. As the infection progressed, viral antigen appeared in an increasing number of cells, and rounded globular cells with long slender processes harboring intense fluorescence were seen. Nuclear fluorescence was not observed in infected monolayers. Polykaryocytes formed within 6 hr after inoculation due to the direct cell-fusing effect of the virus inoculum did not show specific fluorescence. Viral antigen was found, however, in the cytoplasm of multinucleated giant cells in cover slips harvested after new infective virus had been released, and later in the course of infection circular fluorescent inclusions were seen in the cytoplasm of polykaryocytes. Comparable eosinophilic inclusions were observed in hematoxylin and eosin preparations, and acridine orange staining of infected monolayers demonstrated similar inclusions which fluoresced with the color characteristic of single-stranded nucleic acid and were susceptible to digestion with ribonuclease. Visna virus appears to be a ribonucleic acid virus which replicates in the cytoplasm.

Animals↗
PubMed1966

Subacute sclerosing leukoencephalitis: ultrastructure of intranuclear and intracytoplasmic inclusions.

Intranuclear inclusions found in glial cells of two cases of subacute sclerosing leukoencephalitis have been examined in the electron microscope. The inclusions are composed of filamentous tubules 170 to 230 angstroms in diameter, which bear a general resemblance to the intranuclear structures observed in cells infected with measles virus. This finding provides further suggestive evidence that a virus may be involved in the pathogenesis of subacute sclerosing leukoencephalitis.

Cerebellum↗
PubMedDate not supplied

Sodium vanadate inhibits apoptosis in malignant glioma cells: a role for Akt/PKB.

The dual signal hypothesis of apoptosis holds that a common signal can activate both apoptotic and proliferative pathways. The fate of a cell is dependent on which of these two pathways predominates. In the MAPK family of kinases, ERK and JNK have been proposed to mediate apoptosis whereas the PI3K-stimulated kinase, Akt/PKB, has been shown to inhibit apoptosis. The object of this study was to determine the role of these kinases in a glioma model of apoptosis. We have previously shown that K252a induces apoptosis and inhibits kinase activity. In this study we confirm these results and show that the protein tyrosine phosphatase inhibitor sodium vanadate activates ERK, JNK and Akt/PKB, but does not stimulate proliferation. Vanadate did protect T98G cells from K252a-induced apoptosis, an effect that was abolished by addition of the PI3K inhibitor wortmannin. This suggests that PI3K and Akt/PKB may be responsible for mediating vanadate's protective effect on glioma cells. We conclude that the intracellular balance between protein phosphorylation pathways is a critical determinant of both cell proliferation and cell death.

Androstadienes↗