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Volume 17, Number 8—August 2011

Research

Seroprevalence of Trichodysplasia Spinulosa–associated Polyomavirus

Els van der MeijdenComments to Author , Siamaque Kazem, Manda M. Burgers, Rene Janssens, Jan Nico Bouwes Bavinck, Hester de Melker, and Mariet C.W. Feltkamp
Author affiliations: Author affiliations: Leiden University Medical Center, Leiden, the Netherlands (E. van der Meijden, S. Kazem, M.M. Burgers, J.N. Bouwes Bavinck, M.C.W. Feltkamp); Jeroen Bosch Ziekenhuis, ‘s Hertogenbosch, the Netherlands (R. Janssens); National Institute of Public Health and the Environment, Bilthoven, the Netherlands (H. de Melker)

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Figure 3

Cross-competition between trichodysplasia spinulosa–associated polyomavirus (TSV) and Merkel cell polyomavirus (MCV) viral protein 1 (VP1) in serial dilutions of serum samples RTR 108 and RTR 128 from renal transplant recipient patients reactive against TSV VP1 and MCV VP1, the Netherlands. Reactivity was determined by using the VP1 multiplex antibody-binding assay. Samples were preincubated with soluble recombinant glutathione-S-transferase (GST) (black line), GST-MCV VP1 (red line), or GST-TSV

Figure 3. Cross-competition between trichodysplasia spinulosa–associated polyomavirus (TSV) and Merkel cell polyomavirus (MCV) viral protein 1 (VP1) in serial dilutions of serum samples RTR 108 and RTR 128 from renal transplant recipient patients reactive against TSV VP1 and MCV VP1, the Netherlands. Reactivity was determined by using the VP1 multiplex antibody-binding assay. Samples were preincubated with soluble recombinant glutathione-S-transferase (GST) (black line), GST-MCV VP1 (red line), or GST-TSV VP1 (blue line). Values are median fluorescent intensity (MFI) for seroreactivity against TSV VP1 (A and B) or MCV VP1 (C and D).

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