The majority of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected individuals remain paucisymptomatic, contrasting with a minority of infected individuals in danger of death. Here, we speculate that the robust disease resistance of most individuals is due to a swift production of type I interferon (IFNα/β), presumably sufficient to lower the viremia. A minority of infected individuals with a preexisting chronic inflammatory state fail to mount this early efficient response, leading to a delayed harmful inflammatory response. To improve the epidemiological scenario, we propose combining: (i) the development of efficient antivirals administered early enough to assist in the production of endogenous IFNα/β; (ii) potentiating early IFN responses; (iii) administering anti-inflammatory treatments when needed, but not too early to interfere with endogenous antiviral responses.

大多数严重急性呼吸系统综合症冠状病毒2（SARS-CoV-2）感染的个体仍然是有症状的，而少数感染个体有死亡的危险。在这里，我们推测大多数人对疾病的抵抗力强是由于I型干扰素（IFNα/β）的迅速产生，据推测足以降低病毒血症。少数具有预先存在的慢性炎症状态的受感染个体无法进行这种早期有效反应，从而导致延迟的有害炎症反应。为了改善流行病学情况，我们建议结合以下方面：（i）尽早施用有效的抗病毒药以协助内源性IFNα/β的产生；（ii）增强早期IFN反应；（iii）必要时进行抗炎治疗，