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The Journal of Immunology, 1961, 87: 80-89.
Copyright © 1961 by The American Association of Immunologists, Inc.

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A Comparison of Cytopathology Caused by Myxoviruses

I. The Relation of the Infectious Process to Cytopathology1

John P. Bader and Herbert R. Morgan

From the Louis A. Wehle Virus Research Laboratory, Department of Bacteriology, The University of Rochester School of Medicine and Dentistry, Rochester, New York

Abstract

A comparison of cytopathology in HeLa and L cells caused by Newcastle disease virus (NDV), PR8-influenza virus and mumps virus demonstrated that all viruses produced cytopathic effects (CPE) in both cell lines but mumps virus, which failed to lyse L cells. A high virus/cell ratio was required for production of CPE by PR8 virus in HeLa cells and for PR8 virus and NDV in L cells. Replication of infectious virus could be demonstrated only for NDV and mumps virus in HeLa cells, but noninfectious hemagglutinins were produced in both cell lines after infection with high multiplicities of NDV or PR8 virus. The production of these noninfectious hemagglutinins by individual cells was demonstrated by a modification of the hemadsorption technique.

The specificity of the cytopathic action of these myxoviruses was indicated by the facts that the CPE were dependent on adsorption of the viruses to the cells and that when the cell surface was altered by RDE that the viral CPE were prevented. Cellular receptors involved in the viral CPE appeared to be identical for all three viruses since RDE was uniformly effective for all three viruses, and saturation of cells with one virus prevented the adsorption of a second virus.

The CPE of these viruses on HeLa and L cells were shown to involve two stages, the first of which was dissociable by RDE which prevented the CPE. Following this initial stage at 37°C, the initial virus-cell complex proceeded rapidly to a stage which was not affected by RDE or specific antibody since the cells were lysed on further incubation.

Footnotes

Supported by grants from the National Cancer Institute, the National Institutes of Health, United States Public Health Service, and the Nelson B. Delavan Virus Research Fund.







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