Abstract
Increasing evidence suggests that dysregulated immune responses are associated with the clinical outcome of coronavirus disease 2019 (COVID-19). Nucleocapsid protein (NP)-, spike (S)-, receptor binding domain (RBD)- specific immunoglobulin (Ig) isotypes, IgG subclasses and neutralizing antibody (NAb) were analyzed in 123 serum from 63 hospitalized patients with severe, moderate, mild or asymptomatic COVID-19. Mild to modest correlations were found between disease severity and antigen specific IgG subclasses in serum, of which IgG1 and IgG3 were negatively associated with viral load in nasopharyngeal swab. Multiple cytokines were significantly related with antigen-specific Ig isotypes and IgG subclasses, and IL-1β was positively correlated with most antibodies. Furthermore, the old patients (≥ 60 years old) had higher levels of chemokines, increased NAb activities and SARS-CoV-2 specific IgG1, and IgG3 responses and compromised T cell responses compared to the young patients (≤ 18 years old), which are related with more severe cases. Higher IgG1 and IgG3 were found in COVID-19 patients with comorbidities while biological sex had no effect on IgG subclasses. Overall, we have identified diseases severity was related to higher antibodies, of which IgG subclasses had weakly negative correlation with viral load, and cytokines were significantly associated with antibody response. Further, advancing age and comorbidities had obvious effect on IgG1 and IgG3.
Highlights
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), is a newly emerged coronavirus causing huge causality of human [1]
Among the many chronic conditions reported in these COVID-19 patients, cardiovascular disease was likely a comorbidity factor to accelerate COVID-19 disease severity (P = 0.049)
Antibody and cytokine responses have been recently reported in COVID-19 patients [23, 34, 35], their associations with viral pathogenesis and disease development are not clearly understood
Summary
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), is a newly emerged coronavirus causing huge causality of human [1]. SARS-CoV and Middle East respiratory syndrome-coronavirus (MERS-CoV) both induce aberrant pro-inflammatory cytokine and chemokine response, resulting in acute lung injury (ALI), and ARDS [5, 6]. During SARS-CoV-2 infection, elevated IL-6, TNF-α, IL-1β, and inflammatory chemokines including IL-8, IP-10 were correlated with the disease severity and the corresponding agonists were used as therapeutic options for COVID-19 [4, 7]. The coronavirus infection in human commonly triggers various antibody responses, among of which neutralizing antibody (NAb) was broadly elicited in SARS-CoV or MERS-CoV patients and had anti-viral activities [12,13,14,15,16]. During SARS-CoV-2 infection, virus-specific IgG and IgM responses were induced within the first 3 weeks after disease onset and were higher in the severe group than non-severe group [17]. Recent studies have described the immune responses in COVID-19 patients with different clinical outcomes [23,24,25], the associations of antibody with viral load, and with cytokines in the COVID-19 patients remain to be elucidated
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