1887

Abstract

Summary

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.

Loading

Article metrics loading...

/content/journal/jgv/10.1099/0022-1317-35-1-159
1977-04-01
2019-11-22
Loading full text...

Full text loading...

http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-35-1-159
Loading

Most Cited This Month

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error