Infection remains a major challenge after hematopoietic stem cell transplantation [1]. In transplant recipients, reactivation of herpes viruses, especially of the human cytomegalovirus (CMV), is associated with severe and fatal complications. CMV is a life-long persisting virus with a seroprevalence between 45 and 100% in the general adult population [2]. Whereas symptomatic CMV infection of healthy individuals is rare, in immunodeficient patients, such as transplant recipients, CMV infection or reactivation commonly manifests as a life-threatening disease affecting different organ systems. Transplant recipients with CMV viremia are usually treated with antiviral drugs [3]. However, myelotoxicity as well as mutations of the viral DNA sequence may limit the use of these drugs [3–5]. Thus, in selected cases alternative therapeutic options are mandatory. We here present the follow-up of a 21-year-old female with acute myeloid leukemia, who was treated with CMV-specific T cells (virus-specific T cells, VSTs). Written informed patient consent has been obtained. Viral load and cellular CMV immunity were closely monitored for almost 3 years. The patient was transplanted in cytomorphologic complete remission but with cytogenetically minimal residual disease. She received allogeneic peripheral blood stem cells from a 9/10 HLA-matched, unrelated male donor in May 2015. Myeloablative conditioning consisted of fludarabin, carmustine, antithymocyte globulin, and melphalan, and the immunosuppressive regimen included cyclosporine A and budesonide. Anti-infective prophylaxis/therapy included amoxicillin, metronidazole, itraconazole, valganciclovir, cotrimoxazol, calciumfolinate, and pentamidine. She received 9.4× 106 CD34+ cells/kg body weight. Three weeks after peripheral blood stem cell transplantation (PBSCT) the patient suffered from acute graft vs. host disease (GvHD) of the skin (stage 1, grade 1), which did not require systemic treatment. The unrelated donor was CMV IgM-and IgG-negative, and the patient was CMV IgM-negative but IgG-positive. Thus, the recipient was at high risk of CMV reactivation. In July 2015 anti-CMV IgM and IgG became positive in the recipient and the viral load reached up to 1,022,908 copies (1,595,800 IU)/ml (day 35) as shown in Fig. 1. Despite antiviral therapy (sequentially with valganciclovir, ganciclovir, and foscarnet) and CMV-specific immunoglobulins no adequate decrease of the viral load was observed. At the peak of CMV reactivation, the patient suffered from a generalized seizure, which was considered cyclosporinerelated. Treatment with cyclosporine and budesonide was switched to mycophenolate mofetil and prednisone. The patient received levetirazepam and no further seizure occurred.

It was then decided to treat the patient with CMV-specific lymphocytes of her HLA haploidentical sister who was CMV IgG-positive. Manufacturing of CMV-specific T cells was carried out at Hannover Medical School with the CliniMACS® Plus Instrument and GMP PepTivator® HCMVpp65 for antigenic restimulation, as described previously [6, 7]. Enrichment of IFN-γ-secreting CMV-specific T cells was performed by immunomagnetic separation using the CliniMACS Cytokine Capture System (Miltenyi Biotec,