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

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

2020-05-15 microbiology
10.1101/2020.05.15.096719 bioRxiv
Show 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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