Cellular thymidine kinase activity is required for the inhibition of HIV-1 replication by AZT in lymphocytes.
In this report, we provide evidence that the cellular thymidine kinase activity is required for the inhibition of HIV replication by zidovudine (AZT) in lymphocytes. The HSV-1 thymidine kinase protein is not able to substitute for the cellular enzyme, in accord with in vitro data that AZT is poorly phosphorylated by the HSV-derived activity.
Lowy
I
I
Department of Medicine, Columbia University, New York, New York 10032.
Caruso
M
M
Goff
S P
SP
Klatzmann
D
D
D054306:Dideoxynucleotides; D004352:Drug Resistance, Microbial; D015497:HIV-1 / Q000187:drug effects* / Q000254:growth & development; D008214:Lymphocytes / Q000201:enzymology* / Q000382:microbiology; D013937:Thymidine Kinase / Q000378:metabolism*; D013942:Thymine Nucleotides / Q000096:biosynthesis; D014779:Virus Replication / Q000187:drug effects; D015215:Zidovudine / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology*
D054306:Dideoxynucleotides; D013942:Thymine Nucleotides; D015215:Zidovudine; C052873:zidovudine triphosphate; D013937:Thymidine Kinase