Acyclovir Sensitivity and Neurovirulence of Herpes Simplex Virus Type 1 with Amino Acid Substitutions in the Viral Thymidine Kinase Gene, Which Were Detected in the Patients with Intractable Herpes Simplex Encephalitis Previously Reported

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  • Inagaki Takuya
    Department of Virology I, National Institute of Infectious Diseases Department of Life Science and Medical Bioscience, Waseda University Computational Bio Big-Data Open Innovation Laboratory, AIST-Waseda University
  • Satoh Masaaki
    Department of Virology I, National Institute of Infectious Diseases
  • Fujii Hikaru
    Department of Virology I, National Institute of Infectious Diseases
  • Yamada Souichi
    Department of Virology I, National Institute of Infectious Diseases
  • Shibamura Miho
    Department of Virology I, National Institute of Infectious Diseases Department of Pediatrics, The University of Tokyo Hospital
  • Yoshikawa Tomoki
    Department of Virology I, National Institute of Infectious Diseases
  • Harada Shizuko
    Department of Virology I, National Institute of Infectious Diseases
  • Takeyama Haruko
    Department of Life Science and Medical Bioscience, Waseda University Computational Bio Big-Data Open Innovation Laboratory, AIST-Waseda University
  • Saijo Masayuki
    Department of Virology I, National Institute of Infectious Diseases Department of Life Science and Medical Bioscience, Waseda University

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<p>Several cases of herpes simplex encephalitis (HSE) caused by acyclovir (ACV)-resistant herpes simplex virus type 1 (HSV-1) have been reported. Amino acid substitutions of R41H, Q125H, and A156V in the viral thymidine kinase (vTK) gene have been reported to confer ACV resistance. Recombinant HSV-1 clones, containing each amino acid substitution in the vTK gene, were generated using the bacterial artificial chromosome system. A recombinant HSV-1 with the Q125H substitution showed ACV resistance while the R41H or A156V substitutions were ACV-sensitive. Furthermore, the Q125H recombinant HSV-1 was less virulent than the repaired virus, but it maintained neurovirulence in mice at relatively high levels. Substitution of Q125H, which was detected in the neonatal HSE patient, conferred ACV resistance, but the substitutions of R41H and A156V, which were detected in immunocompetent adult HSE patients, did not. This suggests that HSE caused by ACV-resistant HSV-1 might be a very rare event to occur during the course of ACV treatment in immunocompetent patients. Showing resistance to ACV treatment does not always indicate emergence of ACV-resistant HSV-1 in HSE patients.</p>

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