Prolonged KI Polyomavirus Infection in Immunodeficient Child

susceptibilities of Leishmania donovani promastigote and amastigote stages to antileishmanial reference drugs: practical relevance of stage-specifi c differences. Functional cloning of the miltefosine transporter. A novel P-type phospholipid translocase from Leishma-nia involved in drug resistance. of the miltefosine transporter, LdMT, causes miltefosine resistance that is conferred to the amas-tigote stage of Leishmania donovani and persists in vivo. S, et al. Mechanisms of experimental resistance of Leishmania to miltefosine: implications for clinical use. Drug Re-Low plasma membrane expression of the miltefosine transport complex renders Leishmania braziliensis refrac-tory to the drug. To the Editor: Two novel polyomaviruses (PyVs), KIPyV and WUPyV, were identifi ed in respiratory and fecal specimens from children with signs and symptoms of respiratory tract infection (1,2). A review of literature on emerging viruses in transplant recipients indicated that up to 80% of patients harboring these PyVs are co-infected with another respiratory virus, complicating interpretation of positive fi ndings (3). Seroprevalence of KIPyV and WUPyV in healthy blood donors in Germany have been reported to be 67% and 89%, respectively (4). The effect of these viruses in immunocompromised patients is unknown. Some studies report a higher frequency of KIPyV DNA detection in hematopoietic stem cell transplant (HSCT) recipients (5–7) than in immunocompetent patients. In fact, HCST recipients might be more prone to productive infection with KIPyV and WUPyV than to infection with PyVs JC and BK (BKPyV) (5). We report prolonged detection of KIPyV DNA in the respiratory tract of an immunocompromised child. A 12-year-old girl with severe combined immunodefi ciency was admitted to the treatment of progressive respiratory problems and cytomegalovirus (CMV) disease. Although the molecular basis of the immune disorder was unknown, HSCT was indicated because of uncontrolled CMV infection and progressive clinical deterioration. Allogenic HSCT was performed in February 2010. Pretransplant treatments included thyothepa (day −7; 8 mg/kg), fl udarabine (days −6 to −3; 120 mg/m 2), treosulfan (days –6 to – 4; 42 g/m 2), and antithymocyte globulin (days −4 to −2; 45 mg/kg). The patient received bone marrow cells (4.2 × 10 6 CD34-positive cells/ kg) from an 8/10 human leukocyte antigen-matched, CMV-positive, unrelated donor. Graft-versus-host disease prophylaxis consisted of cyclosporine A (from day −1) and methotrexate (days +1, +3, +6; 10 mg/m 2). Leukocyte, granulocyte, and platelet engraftment occurred on days +18, +19, and +32, respectively. Full donor chimera was detected by day +62 (Figure, panel A). Before hospitalization, the child had had …