Figure 2.

Time course of innate immune responses to primary SARS-CoV2 infection may be modulated by BCG-induced trained immunity. Delayed or suboptimal antiviral defenses (A) cannot regulate the progression of SARS-CoV2 infection (high viral load). This may result in the development of cytokine storm (overproduction of proinflammatory cytokines as IL-6, IL-8, TNFα), resulting in the influx of various immune cells such as macrophages, neutrophils, and T cells to trigger to acute respiratory distress syndrome (ARDS) and widespread tissue damage (C). Alternatively, in a BCG-vaccinated individual, trained immunity finely tunes type I IFNs/proinflammatory cytokine response (B) to control the SARS-CoV2 infection (low viral load) and, consequently, prevent ARDS (D).