AI Article Synopsis
- A variety of herpes simplex virus type 1 clones were studied after being exposed to a high dose of brivudin, leading to mutations primarily in the thymidine kinase (TK) genes.
- These mutations included 42% frameshift mutations in homopolymer regions and 58% single nucleotide substitutions that either resulted in stop codons or changed existing codons.
- The A168T substitution was the most frequently selected and showed a link between the genetic changes (genotype), their effects on the virus behavior (phenotype), and how lethal they were in living organisms (in vivo neurovirulence).
Article Abstract
A broad variety of herpes simplex virus type 1 clones was selected under a single round of high-dose selection with brivudin. Mutations in the thymidine kinase (TK) genes consisted of 42% frameshift mutations within homopolymer repeats of G's and C's and single nucleotide substitutions (58%) that produced stop codons (Q261 and R281) or a new codon at the site of the substitution (A168T, R51W, G59W, G206R, R220H, Y239S, and T287 M). The A168T change, associated with an altered TK phenotype, proved to be the most commonly selected substitution. For the different mutants, a correlation between phenotype, genotype, and in vivo neurovirulence was observed.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1082774 | PMC |
| http://dx.doi.org/10.1128/JVI.79.9.5863-5869.2005 | DOI Listing |
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