The pathological processes by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that make the virus a major threat to global health are insufficiently understood. Inefficient viral clearance at any stage is a hallmark of coronavirus disease 2019 (COVID-19). Disease severity is associated with increases in peripheral blood cytokines among which interleukin 10 (IL-10) increases particularly early and independent of patient age, which is not seen in active SARS-CoV infection. Here, we consider the known multi-faceted immune regulatory role of IL-10, both in protecting the lung from injury and in defense against infections, as well as its potential cellular source. While the absence of an IL-10 response in SARS is thought to contribute to early deterioration, we suspect IL-10 to protect the lung from early immune-mediated damage and to interfere with viral clearance in COVID-19. This may further both viral spread and poor outcome in many high-risk patients. Identifying the features of the viral genotype, which specifically underlie the different IL-10 dynamics as an etiological endotype and the different viral load kinetics and outcomes as clinical phenotype, may unveil a new immune evasive strategy of SARS-CoV-2.
【저자키워드】 COVID-19, SARS-CoV-2, lung, viral clearance, Interleukin 10, endotype, 【초록키워드】 coronavirus disease, coronavirus, severity, Infection, cytokine, outcome, viral spread, virus, immune, Peripheral blood, Regulatory, Deterioration, Health, infections, Viral load, Patient, Genotype, age, IL-10, High-risk patients, Immune-mediated, clinical phenotype, cellular, Injury, acute respiratory syndrome, SARS-CoV infection, hallmark, Defense, while, identifying, feature, independent, PROTECT, thought, increase, contribute, absence, interfere, etiological, underlie, increases in, 【제목키워드】 protection, interleukin, Suspected,