PNEUMO-VIRUSES - CELL-SURFACE OF LYTICALLY AND PERSISTENTLY INFECTED-CELLS

Human embryonic lung (MRC-5) feline embryo (FEA), mink lung (MVILu) and monkey kidney (BSC-I) cell infected by respiratory syncytial virus showed characteristic morphological changes when viewed by scanning electron microscopy. The surfaces of respiratory synctial virus-infected cells developed a profusion of slender filaments after 48 h incubation at 31°C. Similar changes in surface morphology were observed in BSC-I cells infected by murine pneumonia virus. Filament production therefore appears to be a common property of pneumo-viruses. Filaments were not observed in cells infected with either syncytial and non-syncytial herpes simplex virus, the cytocidal vesicular stomatitis and Batai (Bunyaviridae) viruses, or the focus-inducing rabbit fibroma virus. Filament production was not observed in cells infected with ts mutants of respiratory syncytial (RS) virus during incubation at the restrictive temperature, or in a persistently infected culture of BSC-I cells at 37°C. The persistently infected cells (the RS ts I/BSC-I line) had some of the characteristics of cells transformed by oncogenic viruses, namely ability to overlap adjacent cells and agglutination by a low concentration of concanavalin A. The speudo-transformed phenotype was temperature-dependent, however, and suppressed by raising the temperature of incubation to 39°C. The presence of virus antigen at the cell surface was similarly temperature-dependent in these cells, diminished at high temperature (39°C) and enhanced at low temperature (31°C), suggesting that the changes in the host cell were the result of insertion of virus protein into the cell membrane. Evidently, persistent infection by a cytoplasmic virus can produce alterations in the host cell usually associated with transformation by nuclear viruses.