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. 2019 Jun 18;8(6):610. doi: 10.3390/cells8060610

Figure 2.

Figure 2

Keratin 23 is upregulated upon HCV challenge. (A) Heatmap of mRNA expression levels of keratins in primary human hepatocytes (PHH) upon HCV challenge (MOI 1). Shown are the mRNA expression levels of three independent donors 6 and 72 h post-infection. As a control for the differential gene expression, PHHs were treated with conditioned medium from Huh-7.5 cells and harvested at the same time points. (B) Comparison of HCV RNA copy numbers in primary human hepatocytes (PHHs) upon HCV infection (MOI 10) in the presence or absence of the polymerase inhibitor 2´CMA (10 μM). PHHs were infected with either mock or HCV Jc1 WT in the presence of dimethyl sulfoxide or 10 mM of 2′CMA and lysed 48 h post-infection. The HCV RNA copy numbers were determined by RT-qPCR and normalized to total RNA. (C) Comparison of KRT23 relative mRNA levels in mock-, HCV-infected (MOI 10), and 2′CMA-treated (10 μM) PHHs 48 hpi. KRT23 mRNA levels were normalized to GAPDH mRNA levels as determined by RT-qPCR. (D) Comparison of HCV RNA copy numbers in Huh-7.5 cells upon HCV infection (MOI 1). Huh-7.5 were left uninfected (mock) or infected with HCV Jc1 WT and lysed at the indicated time points. The HCV RNA copy numbers were determined by RT-qPCR and normalized to total RNA. (E) Analysis of KRT23 relative mRNA level induction in the time course of HCV infection (MOI 1). KRT23 mRNA levels were normalized to GAPDH mRNA levels as determined by RT-qPCR. The KRT23/GAPDH ratio of mock infected samples was arbitrarily set as one. (F) Western blot analysis of KRT23 protein levels in Huh-7.5 cells upon HCV challenge.