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H S GINSBERG

Publications and source records attributed to H S GINSBERG.

At least 37 records · Page 2Linked to original sources
PubMed1959

Intracellular localization of type 4 adenovirus. I. Cellular fractionation studies.

HeLa cells infected with types 1 or 4 adenovirus were separated into cytoplasmic and nuclear fractions by mechanical disruption and differential centrifugation and the quantity of infectious virus in each was determined. The results showed that the majority of infectious virus of both types could be isolated in the cytoplasmic fraction. It was not possible to explain the large amount of type 4 virus in the cytoplasmic fraction by the number of nuclei disrupted in the fractionation procedure, but the amount of type 1 virus in the cytoplasmic fraction could have been contributed by disrupted nuclei. This suggested that there might be a basic difference in the intracellular formation of the two types of virus. The intracellular distribution of complement-fixing antigen was similar to that of infectious virus in type 4-infected cells. Technical difficulties, inherent in cellular fractionation studies, were encountered but did not appear to explain the results obtained.

Adenoviridae↗
PubMed1959

Intracellular localization of type 4 adenovirus. II. Cytological and fluorescein-labelled antibody studies.

HeLa cell cultures infected with adenovirus type 4 were studied by light and phase-contrast microscopy and by the fluorescent antibody technique for visualization of intracellular antigen. The findings were correlated with the growth curve of infectious virus, determined from companion cultures. The results indicated that those cells undergoing characteristic structural changes observable by light microscopy were those which contain viral antigen. The distribution of the majority of the antigen within the infected cells corresponded to that of the regularly aligned granules and crystal-like masses seen in the nuclei of cells in stained and in unfixed cultures. The production of infectious virus was closely correlated with the development of the characteristic nuclear changes.

Adenoviridae↗
PubMed1958

Characteristics on the adenoviruses. III. Reproductive cycle of types 1 to 4.

The strains of types 1 to 4 adenoviruses studied attained maximum combination with host cells, strain HeLa, in 5 to 6 hours. During this adsorption period approximately 75 per cent of the total virus became associated with the host cells. Following adsorption of virus to HeLa cells, these agents underwent cyclic multiplication periods similar to bacterial and other animal viruses. The latent or eclipse period of the multiplication cycle for types 1 and 2 viruses was 17 hours, whereas the types 3 and 4 agents had a latent period 14 to 15 hours in length. The rate of viral propagation during the incremental period was very similar for types 1, 2, and 4 viruses, but was slower for the type 3 agent. During the incremental period of viral propagation newly synthesized virus was not released into the fluid phase of the culture and even after 6 days of viral multiplication when marked cytopathic alterations of the infected HeLa cells had occurred, the spontaneous release was only 2 to 6 per cent of the total virus detectable.

Adenoviridae↗
PubMed1957

Cytological and cytochemical studies of HeLa cells infected with adeno-viruses.

The sequential morphological and cytochemical alterations in HeLa cells infected with adenovirus types 1 to 4 are described. Each of the four viruses studied led to consistent and reproducible cytological changes not observed in uninfected control cultures. All four agents produced striking and characteristic changes in the nuclei of infected cells. Alterations in the cytoplasm, though present, were less marked, particularly in the early stages of infection. In cells infected with type 1 or 2 adenovirus, rounded intranuclear inclusions which progressed from eosinophilic and Feulgen-negative to basophilic and Feulgen-positive, together with a homogeneous glassy, Feulgen-positive nuclear background, were prominent features. Cells infected with type 3 or 4 adenovirus exhibited marked rearrangement of basophilic nuclear material and sharply defined crystal-like inclusions, predominantly intranuclear in location, which also varied from Feulgen-negative to positive. In terms of detailed cytological effects, therefore, the four agents could be divided into two subgroups, viz., types 1 and 2 on the one hand and types 3 and 4 on the other. Measurement of DNA in individual nuclei by means of Feulgen microspectrophotometry revealed the values in infected cells to be increased above the levels of the uninfected controls.

Adenoviridae↗
PubMed1957

Immunohistochemical studies on the interaction between Ehrlich ascites tumor cells and Newcastle disease virus.

Newcastle disease virus infection of Ehrlich ascites tumor cells resulted, after a period of time, in the appearance of intracellular viral antigen which could be demonstrated by the fluorescent antibody technique. This antigen appeared in the cytoplasm of infected cells only after inoculation of cell-virus mixtures into the peritoneal cavities of mice. The latent period prior to the appearance of antigen depended inversely on the number of viral particles adsorbed onto the cells prior to inoculation. The final intensity of staining appeared not to be proportionate to the number of viral particles adsorbed to each cell. The appearance of this antigen was not correlated with a rise of titer of infectious, hemagglutinating, or complement-fixing virus. Viral antigen was demonstrated on the surface of tumor cells after adsorption of NDV onto these cells at 0 degrees C. At appropriate virus:cell ratios, antigen was noted to disappear from the surface at 37 degrees C. in vitro, and in vivo, in the absence of demonstrable elution of virus. The appearance of intracellular viral antigen could not be detected in vitro when tumor cell-NDV mixtures were incubated at 37 degrees C., even when an average of 1550 "infectious particles" had adsorbed to each cell.

Animals↗
PubMed1956

The properdin system and immunity. VI. The inactivation of Newcastle disease virus by the properdin system.

Detailed experiments are presented which indicate that the properdin system is an inhibitor of Newcastle disease virus. Viral inhibition required all known components of the properdin system: properdin, all four components of complement and magnesium; the removal of any one constituent resulted in a loss of inhibition; the replacement of the constituent restored antiviral effect. The inhibition of virus was temperature-dependent. The process of inhibition by serum resulted in a decrease in the amount of properdin available in the serum without any measurable effect on the components of complement. The prolonged incubation of inactive serum-virus mixtures with cation-exchange resin resulted in the restoration of some, but not all, of the hemagglutinating activity of the virus. The requirements of the properdin system and the implication of these findings were discussed.

Animals↗