Nucleotide sequence of thymidine kinase gene of sequential acyclovir-resistant herpes simplex virus type 1 isolates recovered from a child with Wiskott-Aldrich syndrome: Evidence for reactivation of acyclovir-resistant herpes simplex virus
✍ Scribed by Saijo, Masayuki; Suzutani, Tatsuo; Itoh, Kiminari; Hirano, Yoshiki; Murono, Koichi; Nagamine, Masayoshi; Mizuta, Katsumi; Niikura, Masahiro; Morikawa, Sigeru
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 235 KB
- Volume
- 58
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Recurrent acyclovir (ACV)-resistant (ACV-r) herpes simplex virus type 1 (HSV-1) infections occurred in a patient with Wiskott-Aldrich syndrome, an X-linked recessive immunodeficiency syndrome composed of three clinical characteristics of immunodeficiency, thrombocytopenia, and an eczematous dermatitis. The patient had severe and recurrent ACV-r herpes simplex and was treated with vidarabine in a satisfactory manner from 1993 to 1997. During the 4-year observation period, two ACV-sensitive (ACV-s) HSV-1 isolates and five ACV-r HSV-1 isolates were recovered. The nucleotide sequence of the thymidine kinase (TK) gene from these sequential ACV-r isolates was compared with the ACV-s isolates. A single nucleotide deletion of cytosine (C) from homopolymer stretch of four C residues between nucleotide 1061 and 1064 of the open reading frame was found in all ACV-r isolates. No other differences were observed in the TK nucleotide sequence between ACV-s and ACV-r isolates. The TK nucleotide sequences of the two ACV-s isolates were identical to each other and those of the five ACV-r isolates were identical to one another. These results suggest that the ACV-r HSV-1 might have derived from the ACV-s strain in the patient body and that TKassociated ACV-r HSV-1 can reactivate from latency.