Neuroinflammation and EIF2 Signaling Persist despite Antiretroviral Treatment in an hiPSC Tri-culture Model of HIV Infection.

Abstract

(Stem Cell Reports 14, 703–716; April 14, 2020) There are two errors in the originally published version of our manuscript in which “TNFα” was inadvertently replaced by “transforming growth factor α” during copyediting. However, this acronym stands for “tumor necrosis factor α.” This has now been corrected in the online version of the manuscript in the following two places. Original text (in the Summary): “This activation was associated with a persistent increase in transforming growth factor α production by microglia.” Corrected text: “This activation was associated with a persistent increase in tumor necrosis factor α production by microglia.” Original text (in the Results): “Therefore, we quantified the changes in production of relevant cytokines in iMg over the course of infection ± EFZ. Infection led to increased production of several proinflammatory cytokines, specifically IL-1b (p < 0.01), IL-1a (p < 0.05), transforming growth factor α (TNF- α) (p < 0.05), and most prominently, IL-8 (p < 0.01) (Figures 2F–2I).” Corrected text: “Therefore, we quantified the changes in production of relevant cytokines in iMg over the course of infection ± EFZ. Infection led to increased production of several proinflammatory cytokines, specifically IL-1b (p < 0.01), IL-1a (p < 0.05), tumor necrosis factor α (TNF- α) (p < 0.05), and most prominently, IL-8 (p < 0.01) (Figures 2F–2I).” We apologize for the oversight and for any resulting confusion. Neuroinflammation and EIF2 Signaling Persist despite Antiretroviral Treatment in an hiPSC Tri-culture Model of HIV InfectionRyan et al.Stem Cell ReportsMarch 26, 2020In BriefAnderson, Jordan-Sciutto, and colleagues developed an hiPSC-derived tri-culture of microglia, astrocytes, and neurons to investigate the cell-cell interactions during HIV infection and antiretroviral treatment. Infection led to EIF2 signaling activation across all cell types and an especially high inflammatory response and reduced synaptophagocytosis by microglia. In addition, with efavirenz treatment, RhoGDI and CD40 signaling were distinctly activated in the microglia. Full-Text PDF Open Access