Abstract
Coronavirus disease 2019 (COVID-19), triggered by the betacoronavirus SARS-CoV-2, has become one of the worst pandemics ofour time that has already caused more than 250,000 deaths (JHU data-05/06/2020, https://coronavirus.jhu.edu/). Effective therapeutic approaches are urgently needed to reduce the spread of the virus and its death toll. Here, we assess the possibility of using interferon-lambda (IFNλ), a third type of interferon sharing low homology with type I IFNs and IL-10, for treating COVID-19 patients. We discuss the unique role of IFNλ in fine-tuning antiviral immunity in the respiratory tract to achieve optimal protection and minimal host damage and review early evidence that SARS-CoV-2 may impair IFNλ induction, leading to a delayed type I IFN-dominated response that triggers hyperinflammation and severe disease. We also consider the potential windows of opportunity for therapeutic intervention with IFNλ and potential safety considerations. We conclude that IFNλ constitutes a promising therapeutic agent for reducing viral presence and hyperinflammation in a single shot to prevent the devastating consequences of COVID-19 such as pneumonia and acute respiratory distress syndrome (ARDS).
Highlights
Coronavirus disease 2019 (COVID-19), triggered by the betacoronavirus SARS-CoV-2, has become one of the worst pandemics of our time that has already caused more than 250,000 deaths (JHU data-05/06/2020, https://coronavirus.jhu.edu/)
S ARS-CoV-2 first appeared in December 2019 in Wuhan, Hubei, China, when a number of people presented with a disease resembling viral pneumonia, termed COVID-19
Understanding what causes acute respiratory distress syndrome (ARDS) in COVID-19 and developing therapeutic options for preventing it from happening or reducing its intensity is key to saving thousands of lives
Summary
Triggered ARDS is characterized by capillary damage and plasma leakage to the alveolar sacs, which disrupts the blood–air barrier and severely impairs blood oxygenation This can occur directly as a result of viral damage, or indirectly by overactivation of the immune system that triggers the infiltration of immune cells such as neutrophils and macrophages into the lung along with a “cytokine storm”—the excessive or uncontrolled production of cytokines such as TNF, interleukin (IL)-1b, IL-6, IL-12, and IFNc, and chemokines such as IL-8, MCP-1, and IP10. This is, in principle, a protective response to limit virus spread but ends up doing more harm than good.
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