AI Article Synopsis
- COVID-19 is caused by the SARS-CoV-2 virus, which leads to severe cases characterized by a strong inflammatory response and acute respiratory distress syndrome.
- Research has identified that the viral gene ORF3a activates the NF-κB signaling pathway, which is crucial for producing proinflammatory cytokines.
- ORF3a enhances the interaction between two key proteins, IKKβ and NEMO, suggesting it plays an important role in the disease process and our understanding of how SARS-CoV-2 affects the immune response.
Article Abstract
Coronavirus disease 2019 (COVID-19) is a global pandemic caused by SARS-CoV-2 infection. Patients with severe COVID-19 exhibit robust induction of proinflammatory cytokines, which are closely associated with the development of acute respiratory distress syndrome. However, the underlying mechanisms of the NF-κB activation mediated by SARS-CoV-2 infection remain poorly understood. Here, we screened SARS-CoV-2 genes and found that ORF3a induces proinflammatory cytokines by activating the NF-κB pathway. Moreover, we found that ORF3a interacts with IKKβ and NEMO and enhances the interaction of IKKβ-NEMO, thereby positively regulating NF-κB activity. Together, these results suggest ORF3a may play pivotal roles in the pathogenesis of SARS-CoV-2 and provide novel insights into the interaction between host immune responses and SARS-CoV-2 infection.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10009424 | PMC |
| http://dx.doi.org/10.1016/j.virusres.2023.199086 | DOI Listing |
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