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. 2015 Jul 7;7(7):3675–3702. doi: 10.3390/v7072794

Figure 3.

Figure 3

Inhibition of IFN signaling by RABV-P. The interaction of Type I IFN with IFNAR leads to the activation of the JAK tyrosine kinases (Tyk2 and JAK1) resulting in the phosphorylation of STAT1 and STAT2, which form, with IRF9, the complex ISGF3. ISGF3 translocates to the nucleus and induces the expression of ISGs that harbor an ISRE. The binding of Type II IFN to its receptor, IFNGR, results in the phosphorylation of STAT1 by JAK1 and JAK2. pSTAT1 homodimers migrate to the nucleus and bind to the GAS in the promoter region of specific ISGs. The steps counteracted by the RABV-P are indicated: P interacts with STAT1 and STAT2, and thereby blocks IFN signaling by STAT1 sequestration in the cytoplasm and the inhibition of pSTAT1 and ISGF3 binding to DNA promoters.