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Eosinophils protect against SARS-CoV-2 following a vaccine breakthrough infection

Moore, K. M.; Foster, S. L.; Elrod, E. J.; Floyd, K. A.; Williams, M. E.; Kar, M.; Vander Velden, J.; Ellis, M.; Malik, A.; Wali, B.; Lapp, S.; Metz, A.; Bosinger, S. E.; Seder, R. A.; Amara, R. R.; Menachery, V. D.; Kohlmeier, J. E.; Grakoui, A.; Suthar, M. S.

2024-08-10 immunology
10.1101/2024.08.08.607190 bioRxiv
Show abstract

Waning immunity and the emergence of immune evasive SARS-CoV-2 variants jeopardize vaccine efficacy leading to breakthrough infections. We have previously shown that innate immune cells play a critical role in controlling SARS-CoV-2. To investigate the innate immune response during breakthrough infections, we modeled breakthrough infections by challenging low-dose vaccinated mice with a vaccine-mismatched SARS-CoV-2 Beta variant. We found that low-dose vaccinated infected mice had a 2-log reduction in lung viral burden, but increased immune cell infiltration in the lung parenchyma, characterized by monocytes, monocyte-derived macrophages, and eosinophils. Single cell RNA-seq revealed viral RNA was highly associated with eosinophils that corresponded to a unique IFN-{gamma} biased signature. Antibody-mediated depletion of eosinophils in vaccinated mice resulted in increased virus replication and dissemination in the lungs, demonstrating that eosinophils in the lungs are protective during SARS-CoV-2 breakthrough infections. These results highlight the critical role for the innate immune response in vaccine mediated protection against SARS-CoV-2.

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