Abstract
Replication complexes of hepatitis C virus synthesized two major species of viral RNA in vitro, double stranded and single stranded. NS5B nonnucleoside inhibitors inhibited dose dependently the synthesis of single-stranded RNA but not double-stranded RNA. Moreover, replication complexes carrying a mutation resistant to a nonnucleoside inhibitor lost their susceptibilities to the inhibitor.
MeSH terms
-
Benzimidazoles / chemistry
-
Benzimidazoles / pharmacology
-
Benzothiadiazines / chemistry
-
Benzothiadiazines / pharmacology
-
Dose-Response Relationship, Drug
-
Hepacivirus / drug effects*
-
Hepacivirus / genetics*
-
Molecular Structure
-
Mutation
-
RNA, Viral / genetics*
-
RNA, Viral / metabolism
-
Templates, Genetic
-
Viral Nonstructural Proteins / antagonists & inhibitors*
-
Viral Nonstructural Proteins / genetics
-
Viral Nonstructural Proteins / metabolism
-
Virus Replication / drug effects
Substances
-
Benzimidazoles
-
Benzothiadiazines
-
RNA, Viral
-
Viral Nonstructural Proteins
-
benzimidazole
-
NS-5 protein, hepatitis C virus