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. 2019 Jun 28;13(6):e0007537. doi: 10.1371/journal.pntd.0007537

Fig 6. The inhibition of ZIKV infection by TRIM56 is independent of the biogenesis of or regulation by host miRNAs.

Fig 6

(A) Expression of miR-92a and miR-21 in control HEK293T cells (WT) and two Dicer-knockout clonal cell lines (No-Dice (2–20) and (4–25)) was determined by qPCR and normalized to U6 snRNA. Results were representative of two independent experiments. (B and C) WT HEK293T and No-Dice cells were infected by ZIKV MR766 strain (MOI = 1) for indicated time points, followed by qPCR analysis of the kinetics of intracellular ZIKV RNA replication (B) and TCID50 assay of progeny virus production in culture supernatants at 72 h.p.i. (C). Student t-test, *P<0.05. Results were reproduced three times. (D-F) WT HEK293T and No-Dice (4–25) cells were stably transduced with empty vector (Bsr) or Flag-T56 and subsequently infected by ZIKV MR766 strain (MOI = 1) for 72 h. Intracellular expression of viral E and NS5 proteins, action, and Flag-T56 were analyzed by immunoblotting (D), and intracellular ZIKV RNA levels was quantified by qPCR (E). Student t-test, **P<0.01. Progeny virus production in culture supernatants was measured by TCID50 assay (F). Student t-test, **P<0.01. Results in panels D to F were reproduced three times.