EBV DNA levels were measured in whole blood and plasma in both arms using real-time polymerase chain reaction (PCR), up to 48 weeks after baseline (BL). Four lymphomas occurred, a median of 61 weeks [range 40−94 weeks] after randomization at a median CD4 cell count of 396 cells/μL (IQR 234–536 cells/μL). In the IL-2 arm, two patients developed EBV-positive Hodgkin’s lymphoma, and one developed EBV-negative Burkitt-type lymphoma. One patient in the control

group developed EBV-positive non-Hodgkin’s lymphoma. CD25 was negative in all cases. Among the 41 of 55 (control arm) and 44 of 58 (IL-2 arm) patients with detectable EBV DNA in whole blood at both BL and week 48, the median change in EBV DNA between BL and week Alectinib mw 48 was +0.04 log10 copies/ml in both arms (P = 0.7). In plasma, EBV was detected at least once in 22 of 52 controls and 21 of 54 IL-2-treated patients (P = 0.8). IL-2 therapy had no significant effect ABT888 on EBV replication over 48 weeks in these ART-naïve patients. The occurrence of lymphomas did not seem to be associated with IL-2 therapy. “
“Vaccination of HIV-infected patients against the influenza A/H1N1 subtype was proposed as a mandatory precautionary measure during the 2009 pandemic. The immediate cardiovascular effects of the novel vaccine have been largely unexplored. We investigated the impact of vaccination on indices of endothelial function in a cohort of HIV-infected patients. We included

24 HIV-infected patients in a study with a randomized, sham procedure-controlled design. A monovalent, adjuvanted vaccine against influenza A/H1N1 was used in the vaccine Interleukin-2 receptor arm (n=16); patients in the control group (n=8) were subjected to a sham procedure. Endothelial function, as assessed by flow-mediated dilatation (FMD), and inflammatory

markers were assessed prior to and 8 and 48 h post vaccination. FMD deteriorated following vaccination (baseline, 6.5 ± 1.1%; 8 h, 1.1 ± 1.5%; 48 h, 2.0 ± 1.4%; P=0.04). The white blood cell count increased at 8 h and remained elevated at 48 h. Soluble intercellular adhesion molecule-1 levels decreased after vaccination; the maximum decrease was noted at 48 h. Conversely, the sham procedure did not induce changes in endothelial function or inflammatory markers, apart from a reduction in the white blood cell count at 48 h. Acute systemic inflammation induced by vaccination against the influenza A/H1N1 virus resulted in a deterioration in endothelial function in HIV-infected patients, and this effect was sustained for at least 48 h. Our findings may have important implications in view of the high cardiovascular risk that HIV infection carries. The effect of the novel vaccine on endothelial function should be weighed against the immunological protection that it confers. In 2009, the medical community witnessed the world-wide spread of a novel strain of the influenza A virus, the H1N1 subtype, which reached pandemic levels.