Severity of SARS-CoV-2 infection as a function of the interferon landscape across the respiratory tract of COVID-19 patients.
Sposito, B.; Broggi, A.; Pandolfi, L.; Crotta, S.; Ferrarese, R.; Sisti, S.; Clementi, N.; Ambrosi, A.; Liu, E.; Frangipane, V.; Saracino, L.; Marongiu, L.; Facchini, F.; Bottazzi, A.; Fossali, T.; Colombo, R.; Clementi, M.; Tagliabue, E.; Pontiroli, A.; Meloni, F.; Wack, A.; Mancini, N.; Zanoni, I.
Show abstract
The COVID-19 outbreak driven by SARS-CoV-2 has caused more than 2.5 million deaths globally, with the most severe cases characterized by over-exuberant production of immune-mediators, the nature of which is not fully understood. Interferons of the type I (IFN-I) or type III (IFN-III) families are potent antivirals, but their role in COVID-19 remains debated. Our analysis of gene and protein expression along the respiratory tract shows that IFNs, especially IFN-III, are over-represented in the lower airways of patients with severe COVID-19, while high levels of IFN-III, and to a lesser extent IFN-I, characterize the upper airways of patients with high viral burden but reduced disease risk or severity; also, IFN expression varies with abundance of the cell types that produce them. Our data point to a dynamic process of inter- and intra-family production of IFNs in COVID-19, and suggest that IFNs play opposing roles at distinct anatomical sites.
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