Properties of a 9-(2-phosphonylmethoxyethyl)adenine (PMEA)-resistant herpes simplex virus type 1 virus mutant
Language English Country Netherlands Media print
Document type Comparative Study, Journal Article
PubMed
2177316
DOI
10.1016/0166-3542(90)90049-d
PII: 0166-3542(90)90049-D
Knihovny.cz E-resources
- MeSH
- Acyclovir pharmacology MeSH
- Adenine analogs & derivatives pharmacology MeSH
- Drug Resistance, Microbial MeSH
- Bromodeoxyuridine pharmacology MeSH
- Mutation * MeSH
- Organophosphonates * MeSH
- Organophosphorus Compounds pharmacology MeSH
- Virus Replication drug effects MeSH
- Simplexvirus drug effects genetics physiology MeSH
- Vero Cells MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Comparative Study MeSH
- Names of Substances
- 9-(S)-(3-hydroxy-2-(phosphonomethoxy)propyl)adenine MeSH Browser
- Acyclovir MeSH
- adefovir MeSH Browser
- Adenine MeSH
- Bromodeoxyuridine MeSH
- Organophosphonates * MeSH
- Organophosphorus Compounds MeSH
After repeated passages of herpes simplex type 1 (HSV-1) KOS virus in the presence of 9-(2-phosphonylmethoxyethyl)adenine (PMEA) a mutant denoted PMEAr HSV-1 was isolated which grew well in the presence of 50-100 micrograms.ml-1 of the drug. PMEAr HSV-1 was still sensitive to the related phosphonate analogue (S)-9-(3-hydroxy-2-phosphonylmethoxypropyl)adenine (HPMPA). In fact, it was more susceptible to the action of HPMPA than the original virus. PMEAr HSV-1 also retained sensitivity to 5-bromo-2'-deoxyuridine and other, viral thymidine kinase-dependent substances such as (E)-5-(2-bromovinyl)-2'-deoxyuridine. However, PMEAr HSV-1 was much less sensitive to acyclovir, 1-(beta-D-arabinofuranosyl)cytosine and 1-(beta-D-arabinofuranosyl)thymine than the parental KOS virus.
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