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Susceptibility of a Herpes Simplex Virus Ribonucleotide Reductase Null Mutant to Deoxyribonucleosides and Antiviral Nucleoside Analogs
Author(s) -
Yamada Yoshinari,
Yamamoto Naohiko,
Daikoku Tohru,
Nishiyama Yukihiro
Publication year - 1991
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1991.tb01600.x
Subject(s) - ribonucleotide reductase , biology , nucleoside , nucleoside analogue , herpes simplex virus , virology , mutant , famciclovir , dna polymerase , ganciclovir , thymidine , virus , dna , biochemistry , human cytomegalovirus , protein subunit , gene
A herpes simplex virus ribonucleotide reductase (RR) null mutant, ICP6 Δ, exhibited hypersensitivity to hydroxyurea, and to the precursors of allosteric inhibitors of cellular RR. The mutant was also much more sensitive than the parental KOS to all of antiviral nucleoside analogs tested, including acyclovir (ACV), ganciclovir (DHPG) and BVaralJ. Our data indicate that cellular RR is essential for the growth of ICP6 Δ, and suggest that inhibitors of viral RR could act as potentiators of all of anti‐herpetic nucleoside analogs whose targets are viral DNA polymerase.