Fig. 2. A hypothetical figure showing how the timing of interferon responses might control innate and adaptive immunity to SARS-CoV-2.

a | When the type I interferon response to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is early and robust, the viral load is quickly controlled, resulting in mild disease. This is followed by normal-level T cell and B cell responses. This may occur in young people or after low-dose viral exposure. b | When the type I interferon response is delayed or reduced early during infection with SARS-CoV-2, viral replication and spread occur. Severe coronavirus disease 2019 (COVID-19) is accompanied by T cell lymphopenia. Despite this, strong antibody responses are induced. Type I interferon induced late during infection may be detrimental in driving pathological responses. This may occur in older adults or after high-dose viral exposure. c | In those individuals who are either genetically or serologically deficient in type I interferon, the replication of SARS-CoV-2 occurs unopposed, causing severe to life-threatening COVID-19. T cell lymphopenia is observed. Compensatory activation of antibody responses occurs but is insufficient to control disease. d | Early post-exposure prophylaxis with recombinant type I interferon can reduce the viral load of SARS-CoV-2 and hasten recovery. However, this leads to reduced antigen load and reduced adaptive immune responses.