Type I Interferons in COVID-19 Pathogenesis

Simple Summary The innate antiviral immune response is essential to limit virus replication at early stages of infection, thus preventing viral spread and pathogenesis. Nevertheless, viruses have evolved different strategies to evade innate immune control. In this review, we describe recent findings delineating the relationship between SARS-CoV-2 and type I IFN response in vitro and in vivo and report current studies using IFN-based therapy for COVID-19 treatment. Among the many activities attributed to the type I interferon (IFN) multigene family, their roles as mediators of the antiviral immune response have emerged as important components of the host response to Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection. Viruses likewise have evolved multiple immune evasion strategies to circumvent the host immune response and promote virus propagation and dissemination. Therefore, a thorough characterization of host-virus interactions is essential to understand SARS-CoV-2 pathogenesis. Here, we summarize the virus-mediated evasion of the IFN responses and the viral functions involved, the genetic basis of IFN production in SARS-CoV-2 infection and the progress of clinical trials designed to utilize type I IFN as a potential therapeutic tool.

Automated summary

The innate antiviral immune response plays a crucial role in limiting virus replication, while viruses have evolved multiple evasion strategies. Understanding host-virus interactions is essential for comprehending SARS-CoV-2 pathogenesis.