Journal List > Ann Clin Microbiol > v.18(2) > 1078538

Seol, Ko, Kim, Kim, Sung, and Lee: The First Case of Ganciclovir-Resistant Cytomegalovirus Colitis with a 597-600 Deletion in UL97 Gene after Stem Cell Transplantation in Korea

초록

Human cytomegalovirus (CMV) infection has been a major concern in hematopoietic stem cell transplant recipients. Ganciclovir (GCV) resistance results most-ly from mutations within the protein kinase UL97 gene. The three hot spots for GCV resistance (codons 460, 520, and 590-607) were well known. We describe a case of GCV-resistant CMV colitis caused by a 597-600 deletion in UL97 after haploidentical peripheral blood stem cell transplantation (h-PBSCT) in a 46 year-old man with myelodys-plastic syndrome. On post-PBSCT day 28, CMV antigenemia turned positive. Treatment of GCV was started and continued for 12 weeks but CMV antigenemia did not respond to the treatment and CMV colitis was worsened. The UL97 showed the in-frame deletion between codons 597 and 600 by direct sequencing. The treatment was switched to foscarnet and the antigenemia test was consecutively negative twice, and clinical symptoms improved. Despite the recovery of the patient from CMV colitis, the patient expired post-PBSCT day 146 from acute liver failure, hepatorenal syndrome and septic shock. This case is a first report of a deletion 597-600 in CMV UL97 in Korea. A 597-600 deletion in UL97 was responsible for the GCV resistance while preserving susceptibility to foscarnet.

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Fig. 1.
Serial follow-up of cytomegalovirus (CMV) pp65 antigenemia. The duration of antiviral drug administration is illustrated by the bar graph at the top of the figure. Abbreviations: GCV, ganciclovir; FOS, foscarnet.
acm-18-64f1.tif
Fig. 2.
Codons 597-600 deletion and the D605E polymorphism in human cytomegalovirus UL97. *D605E polymorphism.
acm-18-64f2.tif
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