UMMS Affiliation
MassBiologics; Department of Biochemistry and Molecular Pharmacology; Schiffer Lab
Publication Date
2020-08-21
Document Type
Article
Disciplines
Amino Acids, Peptides, and Proteins | Biochemistry | Immunity | Immunology of Infectious Disease | Immunopathology | Immunoprophylaxis and Therapy | Immunotherapy | Infectious Disease | Microbiology | Virus Diseases
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 ACE2 receptor binding, by overlapping the ACE2 structural binding epitope. Furthermore, MAb362 IgA neutralizes both pseudotyped SARS-CoV and SARS-CoV-2 in 293 cells expressing ACE2. When converted to secretory IgA, MAb326 also neutralizes authentic SARS-CoV-2 virus while the IgG isotype shows no neutralization. Our results suggest that 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.
Keywords
COVID-19, SARS-CoV-2, Antibody therapy, Molecular modelling, Mucosal immunology, Viral infection
Rights and Permissions
© The Author(s) 2020. Open Access: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/ licenses/by/4.0/.
DOI of Published Version
10.1038/s41467-020-18058-8
Source
Ejemel M, Li Q, Hou S, Schiller ZA, Tree JA, Wallace A, Amcheslavsky A, Kurt Yilmaz N, Buttigieg KR, Elmore MJ, Godwin K, Coombes N, Toomey JR, Schneider R, Ramchetty AS, Close BJ, Chen DY, Conway HL, Saeed M, Ganesa C, Carroll MW, Cavacini LA, Klempner MS, Schiffer CA, Wang Y. A cross-reactive human IgA monoclonal antibody blocks SARS-CoV-2 spike-ACE2 interaction. Nat Commun. 2020 Aug 21;11(1):4198. doi: 10.1038/s41467-020-18058-8. PMID: 32826914. Link to article on publisher's site
Journal/Book/Conference Title
Nature communications
Related Resources
PubMed ID
32826914
Repository Citation
Monir E, Li Q, Hou S, Schiller Z, Wallace A, Amcheslavsky A, Yilmaz NK, Toomey JR, Schneider R, Ramchetty AS, Ganesa C, Cavacini L, Klempner MS, Schiffer CA, Wang Y. (2020). A cross-reactive human IgA monoclonal antibody blocks SARS-CoV-2 spike-ACE2 interaction. COVID-19 Publications by UMMS Authors. https://doi.org/10.1038/s41467-020-18058-8. Retrieved from https://escholarship.umassmed.edu/covid19/102
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
Included in
Amino Acids, Peptides, and Proteins Commons, Biochemistry Commons, Immunity Commons, Immunology of Infectious Disease Commons, Immunopathology Commons, Immunoprophylaxis and Therapy Commons, Immunotherapy Commons, Infectious Disease Commons, Microbiology Commons, Virus Diseases Commons
Comments
Full author list omitted for brevity. For the full list of authors, see article.