ABSTRACT
COVID-19 is a viral respiratory infection caused by SARS-CoV-2. The immune system plays a pivotal role in disease resolution but can also be detrimental to the clinical outcome in case of unbalanced immune activation. In this study, we have focused on the parallel expression of IL-6, a potent pro-inflammatory cytokine, and IL-10, an important regulator of the immune response, in COVID-19 patients. Using bead-based multiplex immunoassay technology we compared the serum levels of IL-6 and IL-10 in 47 COVID-19 patients with mild, moderate, or severe disease. The serum concentrations of both cytokines were significantly elevated in patients with severe COVID-19, and there was a significant positive correlation between IL-6 and IL-10 in the moderate and severe groups (R=0.6;p< 0.001). Our observations support that IL-6 is one of the driving forces for the cytokine release syndrome in COVID-19 while the immunosuppressive properties of IL-10 in severe disease act as a hindrance to viral clearance.
ABSTRACT
Non-SARS coronaviruses (HCoVs) contribute substantially to seasonal common colds. Their structural homology with SARS-CoV-2 suggests a possible cross-reactivity and cross-protection. The presence of IgG to the most common HCoVs (NL63, 229E, OC43, HKU1) in correlation with RBD-specific IgG and IgA, and the susceptibility to SARS-CoV-2 infection was evaluated in 48 individuals with recently diagnosed moderate SARS-CoV-2 infection (A, n=24) or intensive exposure to SARS-CoV-2 (B, n=24). Anti-S1 IgG for each of the four HCoVs, alongside with RBD-IgG and RBD-IgA were evaluated using ELISA (Creative Diagnostics, USA;Euroimmune, Germany). RBD-specific IgG and IgA were detected in 37% and 71% of group A (average levels 8.5 and 6.8) and 42% and 29% of group B (average levels 3.4 and 4.6 respectively, p < 0.05). IgG specific for NL63, 229E, and OC43 was present in 100.0%, and for HKU-1 - in 94% of tested samples (average index 7.4, 3.9, 4.1, and 2.6, respectively). The levels of IgG to NL63 and 229E did not differ significantly between the groups (7.6 vs.7.2;3.7 vs. 4.1, p > 0.05), nor did correlate with anti-SARS-CoV-2 response. HKU-1-specific IgG was significantly decreased in COVID-19 patients (A) as compared to SARS-CoV-2 resistant donors (B): 1.98vs.3.2, p < 0.01. Curiously, OC43-specific IgG was lower in the group with intensive exposure to SARS-CoV-2 (3.5vs.4.7, p < 0.01), and correlated with RBD-specific IgA (R=0.42, p < 0.05). IgG to seasonal coronaviruses is commonly detected, but only HKU-1-specific IgG was associated with resistance to SARS-CoV-2 infection. OC43-specific IgG may be induced simultaneously with RBD-specific IgA and interfere with SARS-CoV-2 neutralization.