In children who suffer out of hospital cardiac arrest, targeted hypothermia at 33.0 C confers no benefit when compared to targeted normothermia at 36.8 C. Level of evidence: 2B (RCT with wide CIs)Appraised by: Andrew Claxton Citation: Moler FW, Silverstein FS, Holubkov R and the THAPCA Trial Investigators. Therapeutic hypothermia after out-of-hospital cardiac arrest in children. N Eng

BACKGROUND-Targeted temperature management is recommended for comatose adults and children after out-of-hospital cardiac arrest; however, data on temperature management after inhospital cardiac arrest are limited.

Viral FLIPs (vFLIPs) interfere with apoptosis signaling by death-domain-containing receptors in the TNFR superfamily (death receptors). In this study, we show that T cell-specific transgenic expression of MC159-vFLIP from the human Molluscum contagiosum virus blocks CD95-induced apoptosis in thymocytes and peripheral T cells, but also impairs postactivation survival of in vitro activated primary T cells despite normal early activation parameters. MC159 vFLIP impairs T cell development to a lesser extent than does Fas-associated death domain protein deficiency or another viral FLIP, E8. In the periphery, vFLIP expression leads to a specific deficit of functional memory CD8+ T cells. After immunization with a protein Ag, Ag-specific CD8+ T cells initially proliferate, but quickly disappear and fail to produce Ag-specific memory CD8+ T cells. Viral FLIP transgenic mice exhibit impaired CD8+ T cell responses to lymphocytic choriomeningitis virus and Trypanosoma cruzi infections, and a specific defect in CD8+ T cell recall responses to influenza virus was seen. These results suggest that vFLIP expression in T cells blocks signals necessary for the sustained survival of CD8+ T cells and the generation of CD8+ T cell memory. Through this mechanism, vFLIP proteins expressed by T cell tropic viruses may impair the CD8+ T cell immune responses directed against them.