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MicrobiologybioRxiv
Preprint

IgA MAb blocks SARS-CoV-2 Spike-ACE2 interaction providing mucosal immunity

M. Ejemel, Q. Li, S. Hou, Z. A. Schiller, A. L. Wallace, A. Amcheslavsky, N. Kurt Yilmaz, J. R. Toomey, R. Schneider, B. J. Close, D.-Y. Chen, H. L. Conway, M. Saeed, L. A. Cavacini, M. S. Klempner, C. A. Schiffer, Y. Wang

Abstract

COVID-19 caused by SARS-CoV-2 has become a global pandemic requiring the development of interventions for the prevention or treatment to curtail mortality and morbidity. No vaccine to boost mucosal immunity or as a therapeutic has yet been developed to SARS-CoV-2. In this study we discover and characterize a cross-reactive human IgA monoclonal antibody, MAb362. MAb362 binds to both SARS-CoV and SARS-CoV-2 spike proteins and competitively blocks hACE2 receptor binding, by completely overlapping the hACE2 structural binding epitope. Furthermore, MAb362 IgA neutralizes both pseudotyped SARS-CoV and SARS-CoV-2 in human epithelial cells expressing hACE2. SARS-CoV-2 specific IgA antibodies, such as MAb362, may provide effective immunity against SARS-CoV-2 by inducing mucosal immunity within the respiratory system, a potentially critical feature of an effective vaccine.

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