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Basic Characteristics of Mutations
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Mutation Site
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Q125H |
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Mutation Site Sentence
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During the course of therapy, the infection became intractable to the treatment and a mutation in the viral thymidine kinase gene (nucleotide G375T, amino acid Q125H) developed. |
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Mutation Level
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Amino acid level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
|
TK |
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Standardized Encoding Gene
|
UL23
|
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Genotype/Subtype
|
- |
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Viral Reference
|
AB713519;AB713520
|
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Functional Impact and Mechanisms
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Disease
|
Encephalitis, herpes simplex
|
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Immune
|
- |
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Target Gene
|
-
|
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Clinical and Epidemiological Correlations
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Clinical Information
|
Y |
|
Treatment
|
acyclovir |
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Location
|
- |
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Literature Information
|
|
PMID
|
23100343
|
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Title
|
Neonatal herpes encephalitis caused by a virologically confirmed acyclovir-resistant herpes simplex virus 1 strain
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Author
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Kakiuchi S,Nonoyama S,Wakamatsu H,Kogawa K,Wang L,Kinoshita-Yamaguchi H,Takayama-Ito M,Lim CK,Inoue N,Mizuguchi M,Igarashi T,Saijo M
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Journal
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Journal of clinical microbiology
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Journal Info
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2013 Jan;51(1):356-9
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Abstract
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A neonate with herpes simplex virus 1 encephalitis was treated with intravenous acyclovir. During the course of therapy, the infection became intractable to the treatment and a mutation in the viral thymidine kinase gene (nucleotide G375T, amino acid Q125H) developed. This mutation was demonstrated in vitro to confer acyclovir resistance.
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Sequence Data
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-
|