NF-κB signaling promotes SARS-CoV2 infection in human lung epithelial cells

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Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), is responsible for over 660 million infections, and more than 6 million deaths worldwide. There is an increasing need for more treatment options that addresses SARS-CoV-2 infection and its replication. Innate immune pathways including interferon signaling and inflammatory NF-κB signaling are important players in regulating immune responses, these pathways are often targeted by viral pathogens to enhance viral replication, host immune evasion, and host cell survival. The respiratory tract is the major target for SARS-CoV-2; thus, we are exploring the role of innate immune signaling in regulating infection in these cells. We found that both interferon and NF-κB signaling are induced by SARS-CoV-2 infection as measured by increases in transcription factor localization and gene expression. Moreover, pharmacological inhibition of NF-κB signaling but not interferon signaling blocks SARS CoV-2 infection of these respiratory cells. We are exploring how NF-κB signaling impacts viral infection. Indeed, we found that the activity of the NF-κB pathway is independent of interferon signaling. Further mechanistic studies are underway to define the role of NF-κB in coronavirus infection and suggest that inhibitors of the NF-κB signaling pathway may be a novel pharmacological target for the treatment of SARS-CoV-2.

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