New Mechanism of Acyclovir Resistance in Herpes Simplex Virus 1, Which Has a UAG Stop Codon between the First and Second AUG Initiation Codons

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  • Nguyen Phu Hoang Anh
    Department of Virology 1, National Institute of Infectious Diseases, Japan Department of Developmental Medical Sciences, The University of Tokyo, Japan
  • Yamada Souichi
    Department of Virology 1, National Institute of Infectious Diseases, Japan
  • Shibamura Miho
    Department of Virology 1, National Institute of Infectious Diseases, Japan
  • Inagaki Takuya
    Department of Virology 1, National Institute of Infectious Diseases, Japan Department of Life Science and Medical Bioscience, Waseda University, Japan
  • Fujii Hikaru
    Department of Virology 1, National Institute of Infectious Diseases, Japan Department of Microbiology, The Faculty of Veterinary Medicine, Okayama University of Science, Japan
  • Harada Shizuko
    Department of Virology 1, National Institute of Infectious Diseases, Japan
  • Fukushi Shuetsu
    Department of Virology 1, National Institute of Infectious Diseases, Japan
  • Mizuguchi Masashi
    Department of Developmental Medical Sciences, The University of Tokyo, Japan
  • Saijo Masayuki
    Department of Virology 1, National Institute of Infectious Diseases, Japan Department of Developmental Medical Sciences, The University of Tokyo, Japan

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<p>Morphological changes in the structure of the herpes simplex virus 1 (HSV-1) viral thymidine kinase (vTK) polypeptide usually lead to conferring acyclovir (ACV) resistance. HSV-1 I4-2, in which a UAG stop codon is present at the 8th position between the 1st initiation AUG codon (1st position) and the 2nd initiation AUG codon (46th position) of the HSV-1 vTK gene, showed sensitivity to ACV. In contrast, HSV-1 KG111, in which a UAG stop codon was artificially inserted at the 44th position, showed resistance to ACV at 39˚C. The mechanism underlying the difference in the sensitivity profiles was elucidated. The virus recombinants HSV-1-TK(8UAG) and HSV-1-TK(44UAG) containing a UAG stop codon at the 8th and 44th positions counted from the 1st initiation codon, respectively, were generated and tested for susceptibility to antiviral compounds. HSV-1-TK(8UAG) and HSV-1-TK(44UAG) were sensitive and resistant to ACV and BVdU at 37˚C, respectively. The expression level of the truncated vTK translated from the 2nd initiation codon in Vero cells infected with HSV-1-TK(44UAG) was clearly less than that with HSV-1-TK(8UAG) in a temperature-dependent manner. The differences in the antiviral sensitivity profiles were due to the position of the UAG stop codon between the 1st and the 2nd initiation codons.</p>

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