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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
Author(s) -
Saijo Masayuki,
Suzutani Tatsuo,
Itoh Kiminari,
Hirano Yoshiki,
Murono Koichi,
Nagamine Masayoshi,
Mizuta Katsumi,
Niikura Masahiro,
Morikawa Sigeru
Publication year - 1999
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199908)58:4<387::aid-jmv11>3.0.co;2-k
Subject(s) - thymidine kinase , virology , herpes simplex virus , aciclovir , biology , nucleic acid sequence , vidarabine , thymidine , gene , virus , herpesviridae , microbiology and biotechnology , viral disease , dna , genetics , chemotherapy , fludarabine , cyclophosphamide
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 TK‐associated ACV‐r HSV‐1 can reactivate from latency. J. Med. Virol. 58:387–393, 1999. © 1999 Wiley‐Liss, Inc.