Fig. 3
From: Therapeutic strategy targeting host lipolysis limits infection by SARS-CoV-2 and influenza A virus
Dysfunction of cellular glucose transporter systems by virus-induced cell injury, leading to release of FFAs from accumulated lipid droplets for viral palmitoylation and fatty acid oxidation (FAO). a Sequential changes of necroptotic-marker (pMLKL) positive (upper panels) and apoptotic-marker (TUNEL) positive (lower panels) A549 cells infected with IAV PR8 strain at an MOI of 1 FFU determined by immunofluorescence assay (using an antibody against necroptotic marker pMLKL) or TUNEL assay. b, c Sequential glucose uptake into Vero E6 cells infected with SARS-CoV-2 KCDC03 strain at an MOI of 0.1 FFU by measurement of fluorescent glucose using a fluorometer and flow cytometry. d, e Sequential glucose uptake into A549 cells infected with IAV PR8 strain at an MOI of 1 FFU by measurement of fluorescent glucose by a fluorometer and flow cytometry. f Uptake of green fluorescent glucose into Vero E6 cells infected with SARS-CoV-2 at an MOI of 0.1 FFU (upper panels) and A549 cells infected with IAV at an MOI of 1 FFU (lower panels) observed by confocal microscopy. g Graphical representation of inhibitory effects of atglistatin and CAY10499 on intracellular FAO activities in the SARS-CoV-2- and IAV-infected cells at 36 hpi and 24 hpi, respectively. h Representative western blot (left) and quantification (right) of inhibitory effects of atglistatin and CAY10499 on palmitoylation of SARS-CoV-2 S protein in virus-infected Vero E6 cells (MOI = 0.1 FFU) at 36 hpi. All data in the graphs are presented as arithmetic means ± SD from three independent experiments. For statistical analysis, a one-way analysis of variance was carried out with Tukey’s correction for multiple comparisons. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Scale bars = 30 µm
