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. 2017 Aug 2;93(7):449–463. doi: 10.2183/pjab.93.027

Figure 3.

Figure 3.

Incorporation of favipiravir-RTP and GTP into a nascent RNA strand, and inhibition of influenza virus RdRp (Based on Sangawa et al., 201315)). (A) Incorporation of favipiravir-RTP and GTP at the position of G11+2. The 32P-labeled pGEM-7zf (+) DNA run-off transcript with a 5′Cap1 structure (Cap1-pGEM-mRNA), crude influenza virus RdRp containing a viral genome, and nucleotides including favipiravir-RTP were incubated. Reaction products were then electrophoresed. Lane 1–5: Cap1-pGEM-mRNA and crude enzyme solution + 50 µmol/L CTP; Lane 2, 3: Conditions of lane 1 + 100 and 1,000 µmol/L GTP; Lane 4, 5: Conditions of lane 2 + 100 and 1,000 µmol/L favipiravir-RTP. (B) Inhibition of influenza virus RdRp by favipiravir-RTP. The 32P-labeled pGEM-7zf (+) DNA run-off transcript with a 5′Cap1 structure (Cap1-pGEM-mRNA), crude influenza virus RdRp containing a viral genome, and nucleotides including favipiravir-RTP were incubated. Reaction products were then electrophoresed. Lane 1: Cap1-pGEM-mRNA; Lane 2–6: Cap1-pGEM-mRNA + crude enzyme solution; Lane 3–6: Conditions of lane 2 + 50 µmol/L CTP, 100 µmol/L ATP, 50 µmol/L GTP; Lanes 4–6: Conditions of lane 3 + 10, 100, and 1,000 µmol/L favipiravir-RTP. * Elongated RNA was detected when GTP, ATP, and CTP were added to the reaction mixture.