Arenavirus Defective Interfering Particles Mask the Cell-Killing Potential of Standard Virus

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Abstract
Lymphocytic choriomeningitis virus (LCM) and Pichinde virus grew readily and produced cytopathology in MDCK [Madin-Darby canine kidney] and [porcine kidney] PK-15 cells. 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 1-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. DILCM virus could completely prevent standard virus from producing c.p.e. [cytpathic effect] in MDCK monolayers with 1-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. There was only slight interference with the synthesis of standard virus when these cells were pre-treated with DI virus.