Lymphocytic choriomeningitis virus (LCM) and Pichinde virus grew readily and produced cytopathology in MDCK and PK-15 cells. It is known that in these cell lines, the synthesis or function of defective interfering (DI) virus particles is restricted. Survival curves of single MDCK cells infected with low multiplicities of LCM showed one-particle-to-kill kinetics. At high multiplicities of infection, there was a maximum degree of cell-killing, or even a reduction in the amount of cell-killing, depending on how much DI virus was present in a particular standard virus stock. DI LCM virus could completely prevent standard virus from producing c.p.e. in MDCK monolayers with one-particle-to-protect kinetics. It could still prevent killing of the cells when added within a short time after infection with standard virus, but was able to interfere with synthesis of standard virus when added even later. On passage of LCM or Pichinde virus without dilution in MDCK cells, there was no homologous auto-interference. Furthermore, there was only slight interference with the synthesis of standard virus when these cells were pre-treated with DI virus.


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