INHIBITION BY METABOLIC ANALOGUES OF PLAQUE FORMATION BY HERPES ZOSTER AND HERPES SIMPLEX VIRUSES.
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Biomedical subjects
Publications and source records attributed to F RAPP.
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Rapp, Fred (Baylor University College of Medicine, Houston, Tex.). Variants of herpes simplex virus: isolation, characterization, and factors influencing plaque formation. J. Bacteriol. 86:985-991. 1963.-Variants of herpes simplex virus were isolated which differed in plaque size and in virulence for rabbits and mice. Keratitis on the rabbit cornea and generalized disease were associated with the large, but not the small, plaque variants. The large plaque variants were about as neurovirulent as was the parent strain for weanling mice, but the majority of the small plaque variants were only 1% as virulent for mice as was the parent virus. Agar inhibited the formation of plaques by the parent strain and all variants tested; development of plaques was retarded and the number of plaques was approximately 60% less than those developing under an overlay in which methyl cellulose had been substituted for the agar. Rabbit kidney cells and human embryonic lung fibroblasts were more sensitive than mouse embryo fibrolasts to infection with all variants tested.
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The development of measles virus in cultures of both primary human amnion cells and H.Ep.-2 cells has been followed by means of the indirect fluorescent antibody technic and concurrent light and electron microscope observations. The immunofluorescence studies revealed that there is a latent period for development of demonstrable measles virus antigen. In amnion cells the latent period lasted for at least 3 days. In contrast, virus antigen could be detected in H.Ep.-2 cells as early as 12 hours following inoculation. In each cell system virus antigen was seen in either nucleus or cytoplasm of infected cells, or both. Early localization tended to be perinuclear. Intranuclear fluorescence was generally less bright and less widespread than cytoplasmic fluorescence. Giant cells and long cytoplasmic spindle-shaped processes appeared regularly in infected cultures. Infectious virus was liberated into the nutrient fluid but when extracellular virus was inhibited by antibody, spread of infection from cell to cell in the monolayer still continued. Results obtained in concurrent electron microscope studies will be presented separately. Correlation of the results of the immunofluorescence and electron microscope studies suggests the possibility that much of the immunofluorescence observed might be due to antigen in virus precursors or components.
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