Cell killing by simian virus 40: impairment of membrane formation and function

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Abstract
SV-40 infection of the CV-1 line of [African] green monkey kidney cells results in the release of mitochondrial malic dehydrogenase [EC 1.1.1.37] as early as 24 h. Released malic dehydrogenase is detected in the cytoplasm prior to its appearance in the overlay medium. Infected cells lose the ability to consume O2 between 48 and 56 h, and damage to the electron transport system is indicated, but cellular ATP levels remain high as late as 72 h. Infection leads to a stimulation of membrane phospholipid synthesis, which reaches a peak at .apprx. 32 h. This is followed by a severe decline in new membrane synthesis, which correlates in time with the release of cytoplasmic lactic dehydrogenase [EC 1.1.1.27] into the overlay media. Lactic dehydrogenase release precedes the accumulation of trypan blue-stainable cells by .apprx. 6 h. Infection had no effect on the turnover of prelabeled membrane phospholipids. An early SV-40 mutant, tsA58, and a late mutant, tsB11, are both less effective than wild-type virus at causing reduced levels of phospholipid synthesis, enzyme release and the accumulation of trypan blue-stainable cells. Another late mutant, tsB8, is similar to wild-type virus in these respects. At 64 h there is no detectable cell-associated lactic dehydrogenase and nearly all the cells are trypan blue-stainable. Nevertheless, at concentrations of deoxyglucose in the medium below the transport Km, deoxyglucose uptake was similar in infected and control cultures. With higher concentrations of deoxyglucose in the medium, uptake by the infected cultures exceeded that by the control cultures.