|
Basic Characteristics of Mutations
|
|
Mutation Site
|
V173L |
|
Mutation Site Sentence
|
Additional LAM resistance mutations (rtV173L[L], rtL180M[M], and rtM204V[V]) enhanced tenofovir resistance when added to the CYEI mutations. |
|
Mutation Level
|
Amino acid level |
|
Mutation Type
|
Nonsynonymous substitution |
|
Gene/Protein/Region
|
RT |
|
Standardized Encoding Gene
|
P
|
|
Genotype/Subtype
|
C |
|
Viral Reference
|
AB033550
|
|
Functional Impact and Mechanisms
|
|
Disease
|
Hepatitis B, Chronic
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
Y |
|
Treatment
|
- |
|
Location
|
Korea |
|
Literature Information
|
|
PMID
|
33462964
|
|
Title
|
Virologic analysis of tenofovir resistance in a patient with chronic hepatitis B experiencing viral breakthrough during combination treatment with tenofovir disoproxil fumarate and entecavir
|
|
Author
|
Suzuki F,Sezaki H,Hosaka T,Suzuki Y,Fujiyama S,Kawamura Y,Akuta N,Kobayashi M,Saitoh S,Arase Y,Ikeda K,Kobayashi M,Mineta R,Suzuki Y,Kumada H
|
|
Journal
|
Hepatology research : the official journal of the Japan Society of Hepatology
|
|
Journal Info
|
2021 Apr;51(4):503-508
|
|
Abstract
|
Tenofovir disoproxil fumarate (TDF) is widely used to treat hepatitis B virus (HBV) patients worldwide. We previously reported a patient with CHB and cirrhosis in whom viral breakthrough occurred during combination therapy with TDF and entecavir (ETV) against ETV-resistant virus. A recent Korean report showed that two patients with viral breakthrough during treatment with TDF-containing regimens were found to carry five reverse transcriptase (rt) mutations ([rt]S106C[C], rtH126Y[Y], rtD134E[E], rtM204I/V, and rtL269I [I]), with the C, Y, E, and I mutations being associated with tenofovir resistance. We report the clinical course up to September 2019 in our patient, and compare the HBV mutations to those of the two Korean patients. Four mutations (rtS106C, rtD134N/S[N/S], rtM204V, and rtL269I) plus ETV resistance (rtL180M and rtS202G) existed when she developed viral breakthrough during ETV and TDF combination therapy in April 2013. Moreover, three mutations (rtS106C, rtD134N, and rtL269I) existed at baseline. Our patient's father is Korean. Considering these factors, patients with these three or four mutations (CYEI or CN/SI) at baseline could experience tenofovir resistance in addition to lamivudine (LAM) or ETV resistance. In addition, HBV DNA levels fluctuated during tenofovir alafenamide (TAF) and LAM therapy in our patient, although treatment was switched from LAM, TDF, and ETV to LAM and TAF combination therapy in April 2018. In conclusion, three mutations (CN/SI) plus ETV resistance (rtL180M, rtM204V, and rtS202G) can cause tenofovir resistance. Long-term therapy with tenofovir against ETV-resistant virus has the potential to induce viral breakthrough and resistance, necessitating careful follow-up.
|
|
Sequence Data
|
-
|
|
|