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. 2017 Mar 29;13(3):e1006286. doi: 10.1371/journal.ppat.1006286

Fig 9. Schematic summaries of HCoV-229E-mediated chromatin and gene responses and attenuation of NF-κB activity.

Fig 9

(A) Infection of cells with HCoV-229E causes partial degradation of IKKβ, NEMO and IκBα which results in limited nuclear translocation and chromatin recruitment of p65 and other NF-κB subunits and restricted activation of immune modulatory or inflammatory genomic enhancers and NF-κB target genes. The virus also activates a large repertoire of NF-κB-independent virus-specific enhancers and genes which are likely to regulate multiple signaling events and a diverse range of metabolic processes. (B) Results from this study further suggest that HCoV-229E fine tunes basal NF-κB activity at multiple levels to allow optimal replication and to prevent excessive expression of antiviral NF-κB target genes. For details see text. Abbreviations: DMV, double membrane vesicle; E, envelope protein; ERGIC, ER Golgi intermediate compartment; ER, endoplasmic reticulum; M, membrane protein; IκB, inhibitor of NF-κB; IKK, IκB kinase; NEMO, NF-κB essential modifier; N, nucleocapsid protein, RTC, replication-transcription complex; S, spike protein; TNFAIP3, Tumor necrosis factor alpha-induced protein 3.