Researchers review the role of NF-κB activation in the replication of SARS-CoV-2 and the impact of COVID-19 medications on NF-κB activation.
By Dr. Chinta SidharthanOct 25 2023Reviewed by Benedette Cuffari, M.Sc. In a recent study published in the journal Hypertension Research, researchers review the role of nuclear factor kappa B activation in the replication of the severe acute respiratory syndrome coronavirus 2 and the impact of coronavirus disease 2019 medications on NF-κB activation.
However, the rapid development of various COVID-19 vaccines and subsequent global vaccination campaigns have been largely successful in reducing the spread and virulence of SARS-CoV-2. Currently, public health officials have transitioned from preventing SARS-CoV-2 infection to treating COVID-19 cases that arise following infection with new SARS-CoV-2 variants.
The impact of COVID-19 medications on NF-κB activation was also assessed to elucidate how these drugs regulate the uncontrolled inflammatory responses that are characteristic of SARS-CoV-2 infections. The non-canonical pathway does not require the degradation of IκB. However, the phosphorylation of NF-κB inducing kinase and the receptor activator of NF-κB of B lymphocytes is essential for this process.
However, ACE-2 also plays a pivotal role in the RAAS in regulating electrolyte balance and blood pressure. The binding of SARS-CoV-2 to ACE-2 could result in competitive inhibition of the catalytic activity of ACE-2, which could enhance the activation of NF-κB. COVID-19 drugs targeting NF-κB activation Growing evidence suggests that the uncontrolled inflammatory response and cytokine storm that occurs during severe SARS-CoV-2 infection play a significant role in the development of severe post-COVID-19 sequelae. Thus, these hyper-inflammatory responses must be controlled to prevent the multi-organ dysfunction and respiratory distress that often occurs after COVID-19.
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