[Genotyping diagnosis of acyclovir resistant herpes simplex virus]
E Frobert1, D Thouvenot, B Lina
1Laboratoire de Virologie, Centre de Biologie et de Pathologie Est, Hospices Civils de Lyon, 59, Boulevard Pinel, 69677 Bron Cedex, Lyon, France. efrobert@sante.univ-lyon1.fr
Pathologie-Biologie
|October 9, 2007
Summary
Acyclovir (ACV) resistance in herpes simplex virus, often due to thymidine kinase gene mutations, is a problem for immunocompromised patients. Rapid genotyping can detect resistance, enabling faster treatment changes.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Context:
- Acyclovir (ACV) resistance in herpes simplex virus (HSV) poses a significant clinical challenge, particularly in immunocompromised individuals.
- Resistance mechanisms primarily involve mutations in the viral thymidine kinase (TK) or DNA polymerase genes.
- Current detection methods rely on phenotypic testing, which is time-consuming (7-10 days).
Purpose:
- To highlight the need for rapid detection of ACV-resistant HSV.
- To discuss the genetic basis of ACV resistance, focusing on TK gene mutations.
- To advocate for the implementation of direct genotyping from clinical samples.
Summary:
- Herpes simplex virus resistance to acyclovir (ACV) is frequently linked to mutations in the thymidine kinase (TK) gene, often occurring in G/C homopolymer regions.
- These mutations can involve insertions, deletions, or substitutions, impacting viral susceptibility.
- Phenotypic resistance testing is slow, delaying appropriate patient management.
Impact:
- Direct genotyping offers a faster alternative for detecting ACV resistance directly from clinical specimens.
- Rapid diagnosis enables prompt switching to alternative antivirals like foscarnet or cidofovir.
- Improved diagnostic turnaround time can optimize treatment strategies for patients with resistant HSV infections.
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