MDCK cells that normally would have been killed by standard lymphocytic choriomeningitis (LCM) virus were saved either by pre- or co-infection with defective interfering (DI) virus. The ability of these spared cells to produce virus-specific antigen (as well as infectious virus) and resist being killed by standard virus challenge was followed for at least 35 days. During this period both types of cultures displayed unique cycling patterns for the above characteristics. The most striking difference was the longevity of the infections. Cultures exposed to DI particles prior to standard virus became persistently infected, while co-infection with both virus types led to spontaneous curing with no trace of the previous infection. The basis for these dissimilar outcomes was traced to a hitherto undetected non-defective LCM virus (called SP) in the DI virus stocks used to preinfect MDCK cells. SP virus was not present in standard virus stocks but arose in long-term persistently infected L cells that had been initially infected with standard virus. Cloned SP virus shared species-specific antigens with standard virus, was resistant to inhibition by DI virus and was capable of turning self-curing cultures into cultures persistently synthesizing both DI and SP virus.


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