Fig. 5 | Nature Communications

Fig. 5

From: An evolutionary NS1 mutation enhances Zika virus evasion of host interferon induction

Fig. 5

The identity of amino acid 188 of NS1 modulates IFN-β production during ZIKV infection of human cell lines. a Schematics of construction of ZIKV WT and corresponding NS1 mutant viruses. Codons for 188-Ala and 188-Val of NS1 are indicated. b Plaque morphology of recombinant viruses: FSS13025 WT, FSS13025 A188V mutant, PRVABC-59 WT, and PRVABC-59 V188A mutant. c–f IFN-β production of A549 cells (c) or JEG-3 cells (e) in response to ZIKV infection. A549 cells were infected with FSS13025 WT, FSS13025 A188V, PRVABC-59 WT, or PRVABC-59 V188A at an MOI of 0.5. Cells were harvested from 6 to 48 h p.i., total intracellular RNA was isolated, and IFN-β mRNA expression levels were quantified by qRT-PCR. GAPDH was used as a housekeeping gene for normalization. The mRNA levels are shown as fold induction over mock samples. d Intracellular viral RNA copies in A549 cells. f Intracellular viral RNA copies in JEG-3 cells. Error bars indicate standard deviations from three independent experiments. Statistical values were analyzed by unpaired Student’s t-test, *P < 0.05, **P < 0.01, ***P < 0.001, or no significance (n.s.)

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