Dynamics of the Emergence of a Human Cytomegalovirus UL97 Mutant Strain Conferring Ganciclovir Resistance in a Pediatric Stem-Cell Transplant Recipient

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Dynamics of the Emergence of a Human Cytomegalovirus UL97 Mutant Strain Conferring Ganciclovir Resistance in a Pediatric Stem-Cell Transplant Recipient Katharina Göhring, Tobias Feuchtinger, Elfriede Mikeler, Peter Lang, Gerhard Jahn, Rupert Handgretinger, Klaus Hamprecht The Journal of Molecular Diagnostics Volume 11, Issue 4, Pages 364-368 (July 2009) DOI: 10.2353/jmoldx.2009.080153 Copyright © 2009 American Society for Investigative Pathology and Association for Molecular Pathology Terms and Conditions

Figure 1 Clinical course and antiviral treatment of a 4-month old girl with hemophagocytic lymphohistiocytosis after allogeneic stem-cell transplantation from a HLA matched unrelated donor. The patient acquired a HCMV primary infection shortly before and reactivated 60 days after HSCT, thus receiving an intensive antiviral treatment schedule. The gray bars represent the period of antiviral treatment. The Journal of Molecular Diagnostics 2009 11, 364-368DOI: (10.2353/jmoldx.2009.080153) Copyright © 2009 American Society for Investigative Pathology and Association for Molecular Pathology Terms and Conditions

Figure 2 Comparison of UL97 mutation analysis by LightCycler PCR (A-C) and RFLP assay (D-F) of sequential DNA-specimens from blood of a pediatric HSCT recipient with GCV-resistance based on UL97 mutation C603W. Specific melting point analysis and restriction patterns of the investigated patient DNA in comparison with the laboratory wild-type strain AD 169 and a clinical reference strain (5966) or plasmid (pC603W) containing the mutation C603W are shown. The Journal of Molecular Diagnostics 2009 11, 364-368DOI: (10.2353/jmoldx.2009.080153) Copyright © 2009 American Society for Investigative Pathology and Association for Molecular Pathology Terms and Conditions

Figure 3 A: Estimations of sequential DNA viral load data from a pediatric HSCT recipient. Total viral loads are given as well as the deduced viral load ratios of wild-type and mutant strain resulting from a semiquantitative real-time mutation analysis. B: Sequencing analysis of longitudinal blood samples (H12, P697, and H47) with the UL97 mutation C603W are shown in comparison with the laboratory wild-type strain AD169. The Journal of Molecular Diagnostics 2009 11, 364-368DOI: (10.2353/jmoldx.2009.080153) Copyright © 2009 American Society for Investigative Pathology and Association for Molecular Pathology Terms and Conditions