HPV18 E7 selectively antagonizes cGAS‐STING‐triggered NF‐κB activation but not IRF3 activation. (A, B) Schematic diagram of IRF3‐Luc, NF‐κB‐Luc, NFKBIA‐Luc, CXCL8‐Luc, and IFNβ‐Luc constructs. HEK293T cells were transfected with IRF3‐Luc/NF‐κB‐Luc/NFKBIA‐Luc/CXCL8‐Luc/IFNβ‐Luc, pRL‐TK Renilla, Myc‐cGAS and STING‐Flag in the presence or absence of HPV18 E7. (A) Promoter activities and (B) protein expressions were analyzed using a luciferase reporter assay and immunoblotting, respectively. (C) HEK293T cells were transfected with Myc‐cGAS and STING‐Flag in the presence or absence of HPV18 E7. Total mRNA was extracted and analyzed by RT‐qPCR to determine the transcription levels of the indicated genes. Statistical significance was determined using a two‐sided unpaired t‐test (*p < 0.05; **p < 0.01; NS, not significant). The results are shown for N = 3 independent experiments. cGAS‐STING, GMP–AMP synthase‐stimulator of interferon gene; NF‐κB, nuclear factor kappa‐light‐chain‐enhancer of activated B cells; RT‐qPCR, reverse‐transcription quantitative polymerase chain reaction.