Thymidine Transport in Herpesvirus hominis Type 1 and 2 Infected BHK 21 Cells

Abstract

Summary Increase of dThd-uptake 4 to 12 h after infection of BHK or primary rabbit kidney cells with Herpesvirus hominis 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 µm) simple diffusion takes place. The Km of transport of normal BHK or primary rabbit kidney cells (1.4 or 0.5 µm respectively) is not changed after infection. Only the Vmax 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.