Increase of dThd-uptake 4 to 12 h after infection of BHK or primary rabbit kidney cells with of type 1 or 2 can be considered as an early function of the virus genome, because the presence of Cyd-Ara does not prevent the increase of uptake. However, increase of uptake can be prevented by addition of actinomycin D and cycloheximide early in the synthetic cycle.

Two modes of uptake have been differentiated by kinetic analysis: at low substrate concentration dThd is taken up by ‘facilitated transport’, whereas at high substrate concentration (above 2.5 µ) simple diffusion takes place. The K of transport of normal BHK or primary rabbit kidney cells (1.4 or 0.5 µ respectively) is not changed after infection. Only the V increases from 8 to 26.6 pmol in BHK cells or from 2.9 to 9.0 pmol in primary rabbit kidney cells. This indicates that ‘carrier sites’ with identical affinity for dThd-transport are responsible for the increase of transport after infection. This increase of transport is correlated with the induction of a virus coded thymidine kinase (TK) and not with different types of c.p.e. or cellular damage.

Transport of BdUrd increases in a similar manner to that of dThd after infection; transport of dCyd or dUrd increases only slightly, whereas the mechanism of dAdo or Urd uptake by infected cells is quite different.


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