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. 2023 Dec 9;13(12):1766. doi: 10.3390/biom13121766

Figure 1.

Figure 1

Viruses modulate the EGFR signaling network. (A) For entry, gB of HCMV binds to EGFR and induces internalization of EGFR and virus particles. HBV-NTCB interacts with EGFR, facilitating the entry process. EGFR acts as a co-factor on the plasma membrane to facilitate host cell entry in IAV, HEV, and HCV infections. (B) For regulation of the EGFR signaling pathway and EGFR expression, accumulation of EGFR is observed in the nucleus. UL138 of HCMV and LMP1 of EBV induce upregulation of EGFR expression. Conversely, HBx of HBV, UL135 of HCMV, and ICP0 of HSV-1 suppress EGFR production. The expression of MUC5AC is increased by respiratory virus infections such as RV, SARS-CoV-2, IAV, and RSV. The phosphorylation of EGFR is triggered by VACV and JEV infection, and the MAPK/ERK pathway is activated by IAV and HPV-6 infection. IRF-1 is suppressed in RSV infection. In the PI3K/Akt pathway, DENV induces NF-κB activation, whereas the RIDα of AdV inhibits NF-κB. The miR-US5-2 of HCMV inhibits the activation of the Jak/STAT pathway, whereas LMP1 of EBV upregulates STAT activation. (C) For EGFR trafficking with viral proteins into intracellular organelles, E7 of HPV promotes the internalization of EGFR, and EGFR trafficking into endosomes is essential for HCMV and HBV replication. This figure was generated by using a drawing tool available in Microsoft PowerPoint version 2023.