IL-1-mediated inflammation in COVID-19

The COVID-19 pandemic has affected almost every region of the planet and has become the top infectious killer in a very short period, resulting in a pandemic. The rapid spread of SARS-CoV2 and its deadly nature demands urgent identification of drugs and vaccines for efficient treatment of COVID-19 patients. Antibiotic treatment solely is inefficient for eliminating viral infections, and developing a promising vaccine against an unpredictable virus is not an easy task either. Proinflammatory cytokines like IL-1, IL-6, IL-12, TNF-α, and IFN-γ are established to be protective against most infections. However, in COVID-19, hyperproduction of these cytokines in a “cytokine storm” establishes the primary manifestation of the disease as they contribute to widespread tissue injury. Among the other proinflammatory cytokines, the IL-1 superfamily of cytokines, such as IL-1α, IL-1β, IL-18, IL-33, IL-36, and IL-38, plays a significant role in the pathogenesis of the cytokine storm. The inhibitors of IL-1 cytokines have been extensively investigated to limit COVID-19 pathogenesis. Among the IL-1 inhibitors that have been proven to be quite effective to limit the pathogenesis of COVID-19 are the following: anakinra, an IL-1 receptor antagonist; canakinumab, a monoclonal antibody against IL-1β; and rilonacept, an extracellular portion of IL-1 receptor.