Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) shows a high degree of homology with SARS-CoV. They share genes, protein sequences, clinical manifestations, and cellular entry patterns. Thus, SARS research may serve helpful in gaining a better understanding of the current coronavirus disease 2019 (COVID-19) pandemic. Serum antibodies from convalescent patients with SARS collected in 2018 were used to target the recombinant SARS-CoV-2 spike protein via a chemiluminescence microsphere immunoassay. Antibodies of convalescent patients with SARS exhibited serous immune cross-reactivity with the SARS-CoV-2 spike protein. The serous antibodies, excluding S22 of convalescent patients with SARS, did not competitively inhibit the binding of SARS-CoV-2 spike protein to ACE2. T cellular immunity research was conducted in vitro using peripheral blood mononuclear cells (PBMCs) stimulated by pooled peptide epitopes 15 years post-infection. Interferon gamma was detected and the PBMC transcriptomic profile was obtained. The heatmap of the transcriptomic profile showed that mRNAs and circRNAs of the SARS group clustered together after being stimulated by the peptide epitope pool. Differentially expressed mRNAs were most significantly enriched in immunity and signal transduction (P < 0.01). SARS elicits cytokine and chemokine responses, partially consistent with previously published data about COVID-19. Overall, our results indicate that antibodies from convalescent patients with SARS persisted for 15 years and displayed immune cross-reactivity with the SARS-CoV-2 spike protein. The immune status of patients with SARS 15 years post-infection may provide a better understanding of the future immune status of patients with COVID-19.
Highlights
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Considering the homology between the gene and protein sequences of SARS-CoV and SARS-CoV-2, as well as several similar clinical manifestations and cellular entry patterns, we investigated whether SARS-CoV-2 undergoes an immune cross-reactivity with the sera of convalescent patients with SARSCoV infection
There were no significant differences between the groups in terms of sex, age, comorbidities, and laboratory testing except pulmonary fibrosis
Summary
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 is highly homologous to SARS-CoV—the causative agent of the severe acute respiratory syndrome (SARS) outbreak of 2003— and shares 79%–82% of its genome and 95%–100% of its proteome with the latter (Lu et al, 2020; Xu et al, 2020). The most frequent initial symptoms were fever (100%), cough (61%), myalgia (48%), dyspnoea (40%), diarrhoea (31%), and rigor (30%). Initial laboratory data indicated lymphopenia, thrombocytopenia, and elevated aspartate transaminase, alanine aminotransferase, lactic dehydrogenase, and C-reactive protein levels. 40%–45% of the patients with SARS-CoV-2 infection are asymptomatic. COVID-19 causes a few immune disorders such as interstitial lung injury, coagulopathy, and vasculitis (Agricola et al, 2020; Dominguez-Santas et al, 2020; Oda et al, 2020; Ramlall et al, 2020)
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