|
Basic Characteristics of Mutations
|
|
Mutation Site
|
M204V |
|
Mutation Site Sentence
|
Co-treatment of BA and ETV had a more dramatic effect in NA-resistant HBV(rtM204V/rtLl80M) transfected hepG2 cells. |
|
Mutation Level
|
Amino acid level |
|
Mutation Type
|
Nonsynonymous substitution |
|
Gene/Protein/Region
|
RT |
|
Standardized Encoding Gene
|
P
|
|
Genotype/Subtype
|
C |
|
Viral Reference
|
-
|
|
Functional Impact and Mechanisms
|
|
Disease
|
-
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
- |
|
Treatment
|
Entecavir(ETV) |
|
Location
|
China |
|
Literature Information
|
|
PMID
|
28322895
|
|
Title
|
Baicalin benefits the anti-HBV therapy via inhibiting HBV viral RNAs
|
|
Author
|
Huang H,Zhou W,Zhu H,Zhou P,Shi X
|
|
Journal
|
Toxicology and applied pharmacology
|
|
Journal Info
|
2017 May 15;323:36-43
|
|
Abstract
|
BACKGROUND: Although current antiviral treatments (nucleoside analogs, NAs) for chronic hepatitis B virus (HBV) infection are effective in suppressing HBV-DNA replication, their clinical outcomes can be compromised by the increasing drug resistance and the inefficiency in promoting HBsAg/HBeAg seroconversion. OBJECTIVES: In this study, we will explore possible effects and mechanism of a natural product baicalin (BA) with the anti-HBV efficacy of entecavir (ETV), a first-line anti-HBV drug, in HBV-DNA, HBsAg/HBeAg seroconversion and drug-resistance. METHODS: The co-effects of BA and ETV were conducted in wild-type/NA-resistance mutant HBV cell lines and DHBV-infected duckling models. HBV-DNA/RNAs, HBsAg/HBeAg, host factors (hepatocyte nuclear factors) were explored for possible anti-HBV mechanism. RESULTS AND DISCUSSION: BA could significantly enhance and reduced HBsAg and HBeAg in hepG2.2.15, a wild-type HBV cell line. Co-treatment of BA and ETV had a more dramatic effect in NA-resistant HBV(rtM204V/rtLl80M) transfected hepG2 cells. Our study further revealed that BA mainly inhibited the production of HBV RNAs (3.5, 2.4, 2.1kb), the templates for viral proteins and HBV-DNA synthesis. BA blocked HBV RNAs transcription possibly by down-regulating transcription and expression of HBV replication dependent hepatocyte nuclear factors (HNF1alpha and HNF4alpha). Thus, BA may benefit the anti-HBV therapy via inhibiting HBV viral RNAs.
|
|
Sequence Data
|
-
|