Abstract
Lasting immunity following SARS-CoV-2 infection is questioned because serum antibodies decline in convalescence. However, functional immunity is mediated by long-lived memory T and B (Bmem) cells. Therefore, we generated fluorescently-labeled tetramers of the spike receptor binding domain (RBD) and nucleocapsid protein (NCP) to determine the longevity and immunophenotype of SARS-CoV-2-specific Bmem cells in COVID-19 patients. A total of 36 blood samples were obtained from 25 COVID-19 patients between 4 and 242 days post-symptom onset including 11 paired samples. While serum IgG to RBD and NCP was identified in all patients, antibody levels began declining at 20 days post-symptom onset. RBD- and NCP-specific Bmem cells predominantly expressed IgM+ or IgG1+ and continued to rise until 150 days. RBD-specific IgG+ Bmem were predominantly CD27+, and numbers significantly correlated with circulating follicular helper T cell numbers. Thus, the SARS-CoV-2 antibody response contracts in convalescence with persistence of RBD- and NCP-specific Bmem cells. Flow cytometric detection of SARS-CoV-2-specific Bmem cells enables detection of long-term immune memory following infection or vaccination for COVID-19.
Highlights
Coronavirus disease (COVID)-19 is a global health emergency
In subjects with a history of COVID-19, distinct populations of RBDspecific and nucleocapsid protein (NCP)-specific B cells were detected using doublediscrimination (Fig. 1, C). Detection of these populations was highly specific, because neither population was detected in non-infected controls, and the receptor binding domain (RBD)- and NCP-tetramers stained distinct B cell subsets (Fig. 1, C)
We have shown that COVID-19 patients rapidly generate
Summary
The causative agent, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is highly contagious and has infected tens of millions worldwide and caused over 1.2 million deaths since its discovery in Wuhan, China in December 2019 [1, 2]. Mild or asymptomatic in many cases, SARS-CoV-2 infection in the elderly and individuals with chronic health problems can result in severe COVID-19 requiring invasive ventilation or in death [3,4,5,6]. Since early 2020, many insights have been obtained into the pathology of severe COVID-19. It appears that high viral loads induce strong inflammatory responses that cause systemic disease, especially in the elderly and in individuals requiring immunosuppressive treatment [6]. Immunomodulation with corticosteroids has improved survival in hospitalized individuals, and anti-SARS-CoV-2 monoclonal antibody treatments have shown early evidence of alleviating symptoms and decreasing SARS-CoV-2 viral loads in mild disease [7, 8]
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