Fig. 1: Human genome-wide gain-of-function screening identifies host factors regulating ZIKV infection in Huh7 cells. | Nature Communications

Fig. 1: Human genome-wide gain-of-function screening identifies host factors regulating ZIKV infection in Huh7 cells.

From: Gain-of-function genetic screening identifies the antiviral function of TMEM120A via STING activation

Fig. 1

a Schematic of human genome-wide overexpression screen. b Scatter plot of screen candidates. The x-axis is log2 reads count collected from ZIKV infected cells, and the y-axis is log2 fold changes (FC) in reads count collected from ZIKV infected cells relative to uninfected cells. ORFs with Log2FC > 1 and log2 (reads count) > 10 (Red dotted lines) were considered for validation. Reported restriction factors IL27 and well-known type I interferons IFNA2, IFNA4, IFNA6, and IFNA7 are labelled with orange dots. ZIKV restriction factors TEPP and TMEM120A are labelled with blue and red dots, respectively. c Gene ontology biological processes analysis of the top 250 candidates in Supplementary Data 1 using Metascape webserver. d–f Overexpression of IFNA2 (d), IL27 (e), TEPP (f) significantly reduced ZIKV RNA level in Huh7 cells, respectively. Huh7 cells stably expressing HA-FLAG-tagged luciferase or IFNA2, IL27, TEPP were infected with ZIKV at an MOI of 0.1 for 48 h. Cells were then harvested for RT-qPCR. Cellular ZIKV RNA level was normalized to the internal control GAPDH. RT-qPCR data represent the mean ± SEM (n = 3 independent experiments). ***P < 0.001 (unpaired, two-sided Student’s t-test). Exact P values and statistical parameters are provided in Source Data File.

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