A new acycloguanosine-specific supermutant of herpes simplex virus type 1 thymidine kinase suitable for PET imaging and suicide gene therapy for potential use in patients treated with pyrimidine-based cytotoxic drugs

J Nucl Med. 2008 May;49(5):713-20. doi: 10.2967/jnumed.107.046425. Epub 2008 Apr 15.

Abstract

The herpes simplex virus type 1 thymidine kinase (HSV1-tk) gene is widely used as a suicide gene in combination with ganciclovir (GCV) and as a nuclear imaging reporter gene with an appropriate reporter probe. Wild-type HSV1-tk recognizes a variety of pyrimidine and acycloguanosine nucleoside analogs, including clinically used antiviral drugs. PET of HSV1-tk reporter gene expression will be compromised in patients receiving nucleoside-based antiviral treatment. With the use of an acycloguanosine-specific mutant of the enzyme, PET of HSV1-tk reporter gene expression can be successfully performed with acycloguanosine-based radiotracers without interference from pyrimidine-based antiviral drugs.

Methods: The levels of expression of wild-type HSV1-tk and HSV1-A167Ytk, HSV1-sr39tk, and HSV1-A167Ysr39tk mutants fused with green fluorescent protein (GFP) and transduced into U87 cells were normalized to the mean fluorescence of GFP measured by fluorescence-activated cell sorting. The levels of enzymatic activities of wild-type HSV1-tk and its mutants were compared by 2-h in vitro radiotracer uptake assays with (3)H-2'-fluoro-2'-deoxy-1-beta-d-arabinofuranosyl-5-ethyluracil ((3)H-FEAU), (3)H-pencyclovir ((3)H-PCV), and (3)H-GCV and by drug sensitivity assays. PET with (18)F-FEAU and (18)F-9-[4-fluoro-3-(hydroxymethyl)butyl]guanine ((18)F-FHBG) was performed in mice with established subcutaneous tumors, expressing wild-type HSV1-tk and its mutants, followed by tissue sampling.

Results: FEAU accumulation was not detected in HSV1-A167Ysr39tk-expressing cells and xenografts. Lack of conversion of pyrimidine derivatives by the HSV1-A167Ysr39tk supermutant was also confirmed by a drug sensitivity assay, in which the 50% inhibitory concentrations for thymine 1-beta-d-arabinofuranoside and bromovinyldeoxyuridine were found to be similar to those in nontransduced cells. In contrast, we found that HSV1-A167Ysr39tk could readily phosphorylate (3)H-GCV at levels similar to those of wild-type HSV1-tk and HSV1-A167Ytk but showed enhanced activity with (3)H-PCV in vitro and with (18)F-FHBG in vivo.

Conclusion: We developed a new reporter gene, HSV1-A167Ysr39tk, which exhibits specificity and high phosphorylation activity for acycloguanosine derivatives. The resulting supermutant can be used for PET with (18)F-FHBG and suicidal gene therapy protocols with GCV in patients treated with pyrimidine-based cytotoxic drugs.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Acyclovir / metabolism*
  • Acyclovir / pharmacology
  • Animals
  • Antiviral Agents / chemistry
  • Antiviral Agents / metabolism
  • Antiviral Agents / pharmacology
  • Cell Line, Tumor
  • Cytotoxins / chemistry
  • Cytotoxins / metabolism
  • Cytotoxins / pharmacology
  • Ganciclovir / analogs & derivatives
  • Ganciclovir / metabolism
  • Ganciclovir / pharmacology
  • Gene Expression Regulation, Viral / drug effects
  • Genes, Reporter / genetics
  • Genetic Therapy / methods*
  • Guanine / analogs & derivatives
  • Herpesvirus 1, Human / enzymology*
  • Herpesvirus 1, Human / genetics
  • Humans
  • Mice
  • Mutation*
  • Phosphorylation / drug effects
  • Positron-Emission Tomography / methods*
  • Pyrimidines / chemistry
  • Pyrimidines / metabolism
  • Pyrimidines / pharmacology
  • Substrate Specificity
  • Thymidine Kinase / genetics*
  • Thymidine Kinase / metabolism*

Substances

  • 9-(4-fluoro-3-hydroxymethylbutyl)guanine
  • Antiviral Agents
  • Cytotoxins
  • Pyrimidines
  • Guanine
  • Thymidine Kinase
  • pyrimidine
  • Ganciclovir
  • Acyclovir