期刊
VIRUSES-BASEL
卷 15, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/v15112229
关键词
SARS-CoV-2 ORF3a; NF-kappa B; TRAF proteins; inflammation
类别
This study investigated the roles of the SARS-CoV-2 protein ORF3a in binding to TRAF proteins and activating NF-kappa B. The results suggest that ORF3a can activate NF-kappa B through alternative mechanisms.
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has caused a global pandemic of Coronavirus Disease 2019 (COVID-19). Excessive inflammation is a hallmark of severe COVID-19, and several proteins encoded in the SARS-CoV-2 genome are capable of stimulating inflammatory pathways. Among these, the accessory protein open reading frame 3a (ORF3a) has been implicated in COVID-19 pathology. Here we investigated the roles of ORF3a in binding to TNF receptor-associated factor (TRAF) proteins and inducing nuclear factor kappa B (NF-kappa B) activation. X-ray crystallography and a fluorescence polarization assay revealed low-affinity binding between an ORF3a N-terminal peptide and TRAFs, and a dual-luciferase assay demonstrated NF-kappa B activation by ORF3a. Nonetheless, mutation of the N-terminal TRAF-binding sequence PIQAS in ORF3a did not significantly diminish NF-kappa B activation in our assay. Our results thus suggest that the SARS-CoV-2 protein may activate NF-kappa B through alternative mechanisms.
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