BackgroundEarly antiretroviral treatment (ART), haemopoietic stem-cell transplantation (HSCT), and long-term immune suppression are promising strategies for control of HIV infection, which could potentially allow ART interruption. Here we discuss a patient with HIV infection who received early intensified ART and underwent HSCT for aplastic anaemia. Case presentationA 12-year-old boy with aplastic anaemia acquired HIV infection through platelet transfusion while being treated with oral cyclosporine (10 mg/kg per day), prednisone (1 mg/kg per day), and subcutaneous filgrastim (5 μg/kg per day). Diagnosis was confirmed with a detectable plasma viral load of 508 000 copies per mL. Early ART was started 30 days after HIV infection (zidovudine/lamivudine, lopinavir/ritonavir, intensified with enfuvirtide). Because of HIV infection, physicians decided to postpone HSCT. Cyclosporine was substituted by mycophenolate mofetil (18 mg/kg per day) after 70 days of HIV infection. Plasma viral load was undetectable (<40 HIV RNA copies per mL) after 4 months of ART. After 250 days of HIV infection, the patient underwent HSCT from a sibling donor with an identical HLA genotype (A*02:01:01:01/02:01:01:01; B*41:01/27:05:02; C*02:02:02/17:01:01:01). Both were heterozygous for the CCR5Δ32 mutation. The conditioning regimen consisted of antithymocyte globulin (5 mg/kg per day) and cyclophosphamide (50 mg/kg per day) on day −5 to day −2, and intravenous cyclosporine (5 mg/kg per day) on day −1. Leucocyte engraftment was confirmed (day 9) and mycophenolate was continued for 2 years. Plasma viral load remained undetectable for 3 years. During this period, the patient did not show symptoms of aplastic anaemia, graft-versus-host disease, opportunistic infections, or serious side-effects linked to immunosuppression. At this point (aged 15 years), the patient arrived at our institution, where we started a follow-up protocol after acquiring informed consent from the patient and his parents. The patient had an indeterminate Western blot, negative HIV-ELISA, undetectable plasma viral load, a CD4 count of 766 cells per μL, and a proviral load of 2·88 DNA copies in peripheral blood memory CD4+ T cells (assay detection limit of 2·6 DNA copies). We started a programmed ART interruption protocol. Plasma viral load remained undetectable for 9 days. However, at day 14 the patient had a plasma viral load of 16 566 copies per mL and developed herpes zoster. ART was restarted at day 16 (plasma viral load of 440 307 copies per mL) with a regimen of tenofovir, emtricitabine, and efavirenz. Chimaerism was 89% after 56 months of HSCT. At present (aged 17 years), the patient is well and without symptoms of aplastic anaemia or HIV infection (undetectable plasma viral load and a CD4 count of 990 cells per μL). Consent was acquired from the patient's representatives to publish these data. InterpretationThis case emphasises that early and intensified ART, HSCT, and long-term immune suppression do not assure HIV control after ART discontinuation. Our patient was unable to control HIV infection without ART even though both he and the donor had the HLA B*27:05 allele and were heterozygous for the CCR5Δ32 mutation. HIV plasma viral load rebound could have been caused by remaining infected cells of the recipient because 100% chimerism was not achieved. Other factors to be considered are the absence of graft-versus-host disease, as well as conditioning and maintenance regimens and their potential effects on latently infected cells when compared with recently reported cases. FundingThis work was supported by grants from the Mexican Government (Comisión de Equidad y Género de la Honorable Cámara de Diputados de la LXI Legislatura de México), and Fundación México Vivo (http://www.mexicovivo.org/).