GA/18β doses show different immunomodulation effects
inflammation, infection
INFLAMMATION, SARS-COV-2 INFECTION, COURSE OF ILLNESS, INFECTION
While the modulation of IL-17A and IL-2 remains a shared outcome of treatments, important differences in immune system modulation across doses were observed. In particular, dose A exhibited a more robust immune system modulation compared to dose B, observed as non-significant increases in detected inflammatory interleukins over time. This modulation effect might be linked to IgM-mediated signaling pathways. The initial surge in IgM could potentially regulate interleukin concentrations, preventing cytokine imbalances (Conversely, though IL-10 interleukin levels were comparable between dose A and B during drug administration, an early and modest IL-10 increase on day 5 followed by its subsequent significant reduction was detected in group A (While treatment A tended to maintain interleukin levels relatively close to baseline (100%) during the course of illness, the higher GA/18β dose induced an early increase in two cytokines with reported antiviral activity, namely IFN-γ and IL-12 interleukins. IFN-γ’s ability to hinder viral replication and exhibit anti-inflammatory properties suggests that its elevation induced by dose B might play a pivotal role in slowing down viral replication, limiting spread, and mitigating the early-stage inflammation response to SARS-CoV-2 infection (The significant induction of IFN-γ in the initial days, as observed in group B, could potentially inhibit Th17 cell formation (As IL-12 plays a vital role in the modulation of cytokines and T cell subsets (The induction of IFN-γ in plasma and other interleukins with antiviral activity is not commonly observed in patients diagnosed with moderate-severe COVID-19; instead, they tend to decline in the early days of infection (