Reduction of IL-17 levels by dose B in SARS-CoV-2 infected subjects could probably result from two different pathways: inhibition of the HMGB1-mediated inflammation response, as GA and 18β can directly bind to HMGB1 (2, 8), and a possible inhibition of the viral infection in the early stages, attributed to the antiviral activity produced by early IFN-γ release (55). Here, HMGB1 is linked to viral infectious disease.