Fig. 1: Screening of the EV-derived EBV tegument protein BRRF2 as an inhibitor of the cGAS-STING-mediated signaling pathway. | Nature Communications

Fig. 1: Screening of the EV-derived EBV tegument protein BRRF2 as an inhibitor of the cGAS-STING-mediated signaling pathway.

From: Extracellular vesicles derived EBV tegument protein BRRF2 suppresses cGAS phase separation to promote anti-viral innate immune evasion

Fig. 1

A Protocol for EV isolation and purification from the EBV+ CNE2 cell line. B EV isolation and purification from EBV+ CNE2 cells treated with or without NaB and TPA. Electron microscopy was used to identify EVs and viruses. The experiment was performed as three independent biological replicates. Representative images was shown. C EV isolation and purification from EBV+ CNE2 cells treated with or without NaB and TPA. Western blotting was used to detect EV markers (HSP70, CD63 and CD9) and an EBV-encoded protein marker (EBV-gB). Source data are provided as a Source Data file. D The concentration and size distribution of EVs from EBV+ CNE2 cells treated with or without NaB or TPA were measured using NTA. E EBV viral proteins were sorted by the suppression of cGAS-STING-mediated signaling. HEK293T cells were cotransfected with cGAS, STING, the IFNβ reporter (0.1 μg), the pRL-TK reporter (0.01 μg), and the indicated EBV viral protein plasmids (0.1 μg). The cells were harvested for dual-luciferase assays at 24 h after transfection. The experiment was performed as three independent biological replicates. The data are plotted as the means ± SEMs. F A Venn diagram was constructed to screen EV-derived EBV-encoded proteins involved in suppressing cGAS-STING-mediated signaling.

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