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A single intranasal administration of AdCOVID protects against SARS-CoV-2 infection in the upper and lower respiratory tracts

The coronavirus disease 2019 (COVID-19) pandemic has illustrated the critical need for effective prophylactic vaccination to prevent the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Intranasal vaccination is an attractive approach for preventing COVID-19 as the nasal mucos...

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Bibliographic Details
Published in:Human vaccines & immunotherapeutics 2022-11, Vol.18 (6), p.2127292
Main Authors: Schultz, Michael D., Suschak, John J., Botta, Davide, Silva-Sanchez, Aaron, King, R. Glenn, Detchemendy, Thomas W., Meshram, Chetan D., Foote, Jeremy B., Zhou, Fen, Tipper, Jennifer L., Zhang, Jianfeng, Harrod, Kevin S., Leal, Sixto M., Randall, Troy D., Roberts, M. Scot, Georges, Bertrand, Lund, Frances E.
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Language:English
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Summary:The coronavirus disease 2019 (COVID-19) pandemic has illustrated the critical need for effective prophylactic vaccination to prevent the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Intranasal vaccination is an attractive approach for preventing COVID-19 as the nasal mucosa is the site of initial SARS-CoV-2 entry and viral replication prior to aspiration into the lungs. We previously demonstrated that a single intranasal administration of a candidate adenovirus type 5-vectored vaccine encoding the receptor-binding domain of the SARS-CoV-2 spike protein (AdCOVID) induced robust immunity in both the airway mucosa and periphery, and completely protected K18-hACE2 mice from lethal SARS-CoV-2 challenge. Here we show that a single intranasal administration of AdCOVID limits viral replication in the nasal cavity of K18-hACE2 mice. AdCOVID also induces sterilizing immunity in the lungs of mice as reflected by the absence of infectious virus. Finally, AdCOVID prevents SARS-CoV-2 induced pathological damage in the lungs of mice. These data show that AdCOVID not only limits viral replication in the respiratory tract, but it also prevents virus-induced inflammation and immunopathology following SARS-CoV-2 infection.
ISSN:2164-5515
2164-554X
2164-554X
DOI:10.1080/21645515.2022.2127292