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Recurrent aciclovir‐resistant herpes simplex in a child with Wiskott–Aldrich syndrome
Author(s) -
Masayuki Saijo,
Tatsuo Suzutani,
K Murono,
Yoshiko Hirano,
Kiminari Itoh
Publication year - 1998
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1998.02374.x
Subject(s) - aciclovir , vidarabine , herpes simplex virus , medicine , virology , herpesviridae , virus , surgery , viral disease , chemotherapy , fludarabine , cyclophosphamide
A boy with Wiskott–Aldrich syndrome suffered from thymidine kinase (TK)‐altered and aciclovir‐resistant herpes simplex virus type 1 (HSV‐1) skin infections. He presented with severe herpes simplex around the left eye in March 1993 at the age of 8 years. HSV‐1 strain TAS was isolated and was shown to be susceptible to aciclovir (50% inhibitory concentration (IC 50 ) 0.23 μg/mL). He was treated with intravenous (i.v.) high dose aciclovir, 2 mg/kg per h, which produced an improvement. About 1 year later (May 1994), a severe herpes simplex infection appeared on his face, arm, genitalia, back and foot. Treatment with i.v. aciclovir, 2 mg/kg per h, was initiated, but the skin lesions did not improve. HSV‐1 strain TAR was isolated and was shown to be resistant to aciclovir (IC 50 36 μg/mL). HSV‐1 TAR and TAS were susceptible to vidarabine (IC 50 4.4 and 2.9 μg/mL, respectively). The skin lesions were treated with i.v. vidarabine, 15–20 mg/kg per day, and healed satisfactorily. However, in March 1995, the patient again experienced a severe herpes simplex infection around the left eye. HSV‐1 strain R95 was isolated and was shown to be resistant to aciclovir (IC 50 36 μg/mL). Diminished sensitivity of HSV‐1 TAR and R95 to aciclovir was associated with reduced viral TK activity and loss of aciclovir phosphorylation activity.