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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 PLoS+One 2022 ; 17 (4): e0266412 Nephropedia Template TP
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An endogenously activated antiviral state restricts SARS-CoV-2 infection in differentiated primary airway epithelial cells #MMPMID35436306
Broadbent L; Bamford CGG; Lopez Campos G; Manzoor S; Courtney D; Ali A; Touzelet O; McCaughey C; Mills K; Power UF
PLoS One 2022[]; 17 (4): e0266412 PMID35436306show ga
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of the coronavirus disease-19 (COVID-19) pandemic, was identified in late 2019 and caused >5 million deaths by February 2022. To date, targeted antiviral interventions against COVID-19 are limited. The spectrum of SARS-CoV-2 infection ranges from asymptomatic to fatal disease. However, the reasons for varying outcomes to SARS-CoV-2 infection are yet to be elucidated. Here we show that an endogenously activated interferon lambda (IFNlambda1) pathway leads to resistance against SARS-CoV-2 infection. Using a well-differentiated primary nasal epithelial cell (WD-PNEC) culture model derived from multiple adult donors, we discovered that susceptibility to SARS-CoV-2 infection, but not respiratory syncytial virus (RSV) infection, varied. One of four donors was resistant to SARS-CoV-2 infection. High baseline IFNlambda1 expression levels and associated interferon stimulated genes correlated with resistance to SARS-CoV-2 infection. Inhibition of the JAK/STAT pathway in WD-PNECs with high endogenous IFNlambda1 secretion resulted in higher SARS-CoV-2 titres. Conversely, prophylactic IFNlambda treatment of WD-PNECs susceptible to infection resulted in reduced viral titres. An endogenously activated IFNlambda response, possibly due to genetic differences, may be one explanation for the differences in susceptibility to SARS-CoV-2 infection in humans. Importantly, our work supports the continued exploration of IFNlambda as a potential pharmaceutical against SARS-CoV-2 infection.