HSV susceptibility to acyclovir - genotypic and phenotypic characterization.
Raksha Vikas1, Suresha G Prabhu1, Piya P Mudgal1
1Manipal Centre for Virus Research, Manipal Academy of Higher Education (deemed to be University), Manipal, Karnataka, India.
Antiviral Therapy
|December 4, 2018
Summary
Drug-resistant herpes simplex virus (HSV) infections are a concern. This study identified two new amino acid changes in HSV-1, A37V and H283N, which remain susceptible to acyclovir (ACV).
Area of Science:
- Virology
- Molecular Biology
- Antimicrobial Resistance
Background:
- Drug-resistant herpes simplex virus (HSV) infections pose a significant clinical challenge, particularly for immunocompromised individuals.
- Acyclovir (ACV) is a primary antiviral medication used to treat HSV infections.
Purpose of the Study:
- To detect acyclovir (ACV) susceptibility in clinical samples of herpes simplex virus (HSV).
- To investigate potential genetic markers associated with ACV susceptibility in HSV.
Main Methods:
- Genotypic analysis of the UL23 (thymidine kinase) gene in 13 HSV clinical samples (5 HSV-1, 8 HSV-2).
- Confirmatory phenotypic assay using the plaque reduction technique to determine ACV susceptibility.
- Sequencing of the UL23 gene to identify novel mutations.
Main Results:
- Two novel amino acid changes, A37V and H283N, were identified in HSV-1 positive samples.
- These HSV-1 samples with the novel changes demonstrated susceptibility to acyclovir (ACV), with a half maximal effective concentration (EC50) of 1.5 µM.
- The identified changes were found in patients with unknown immune status and one immunocompromised patient.
Conclusions:
- The novel amino acid changes A37V and H283N in HSV-1 may represent natural polymorphisms within the HSV-UL23 gene.
- These polymorphisms do not appear to confer acyclovir resistance in the studied clinical isolates.
- Further research is warranted to understand the full implications of these genetic variations on HSV antiviral susceptibility.
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