Human type-I interferon omega holds potent antiviral properties and promotes cytolytic CD8 + T cell responses
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The type-I interferon family is well known for its critical role in innate immunity. It comprises several members, among which IFN-α2 and IFN-β are the most extensively studied, with important antiviral and immune-modulatory functions. Recent findings linking autoantibodies against type-I interferons to severe COVID-19 suggest a potential role for IFN-ω in combating SARS-CoV-2 infection. However, little is known about human IFN-ω, as most research on this interferon has been conducted in feline models. Here, we demonstrate that human IFN-ω is secreted at levels comparable to those of IFN-α2 or IFN-β upon stimulation with inflammatory agonists and triggers a robust antiviral response, inhibiting SARS-CoV-2 infection in vitro . Moreover, IFN-ω enhances the effector functions of antigen-specific CD8 + T cells primed de novo from healthy donor cells, highlighting its capacity to promote strong cellular immunity. Our results position IFN-ω as a key member of the type-I interferon family, with promising potential for therapeutic and vaccine applications.
Author Summary
Type-I interferons are pleiotropic cytokines, including IFN-α and IFN-β, which are well known for their antiviral activities. Here, we report on the functional characteristics of human IFN-ω, a neglected member of the type-I IFN family, which has primarily been studied in feline models. We show here that human IFN-ω induces intense downstream signaling in cells resulting in the upregulation of antiviral genes, and efficient restriction of SARS-CoV-2 replication. IFN-ω also promotes the acquisition of strong cytolytic functions by antigen primed CD8 + T cells. Overall, our findings portray human IFN-ω as a major antiviral molecule, similar to the well-studied and highly effective IFN-α 2 . The secretion of IFN-ω upon infection is likely to be crucial for effective control of multiple viruses, advocating for its use in therapeutic approaches in humans.
