Depending on passage history, strain WE infectious LCM virus either damages L cells more or less severely or leaves them morphologically intact. Correspondingly, the plaques which are formed on L cell monolayers are of different appearance, ranging from intensely turbid to clear. Multiplication of LCM virus in certain mouse organs profoundly affects plaque characteristics. The brain, for instance, favours lytic variants while the spleen supports the replication of virus which forms turbid plaques. This statement holds if virus taken from organs of persistently infected mice or virus passaged from mouse to mouse is analysed and is true also if the initial preparation contains virus forming predominantly either clear or turbid plaques on L cell monolayers. Selection is not rapid and not absolute. It may take months of multiplication before a final state is reached, and even then the number of characteristic plaques is usually in great excess of the rest but never reaches 100%. Cloning procedures may alter the proportions, but with our experimental conditions no plaque has ever been isolated which would retain its characteristics upon passage. Differences of plaque type morphology were not reflected in differences of pathogenic properties, and both clear and turbid variants caused persistent infection if used to infect newborn mice and led to disease with signs of neurological involvement and death if inoculated intracerebrally into adult animals.


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