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. 2023 Oct 20;10(11):ofad516. doi: 10.1093/ofid/ofad516

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© The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — EBV-miR-BART17-3p downregulated the RLR pathway and promoted EBV gene expression. A and B, The expression levels of EBV-miR-BART17-3p and genes in the RLR pathway, including IRF3, IRF7, IFNB, RIG-1, and TRAF3, in 18 NK-cell samples from patients. C, The protein expression levels of DDX3X and representative EBV lytic/latent proteins (BZLF1, EBNA1, LMP1) were determined in NKYS cells transfected with EBV-miR-BART17-3p negative controls and mimics by Western blotting. D, The transcriptional levels of EBV latent genes (LMP1, LMP2A, EBNA1), EBV immediate early lytic genes (BZLF1, BRLF1), EBV early lytic genes (BMRF, BGLF5), and late lytic genes (BILF1, GP350) were determined in NKYS cells transfected with EBV-miR-BART17-3p negative controls and mimics by real-time polymerase chain reaction. Statistical analysis was performed with analysis of variance. Correlation was evaluated in terms of the Spearman correlation coefficient. NS, not significant (P > .05). ****P < .0001. Data are presented as mean ± SD. EBV, Epstein-Barr virus; NC, negative control; NK, natural killer; RLR, RIG-I–like receptor.