Eosinophils rapidly decrease in the peripheral blood of patients during COVID-19, and eosinopenia has been correlated with disease severity. These clinical observations suggest that eosinophils may play a functional role in the response to SARS-CoV-2 infection. Murine studies have shown that eosinophils can be recruited to the lungs in response to infection with respiratory viruses, including RSV and influenza and parainfluenza viruses, yet the role of eosinophils in the lungs in response to SARS-CoV-2 infection is unknown. Here, we used a two-pronged approach employing mouse models of SARS-CoV-2 infection to study the role of eosinophils in the antiviral immune response and viral control and clinical samples to assess eosinophilia and eosinophil activation in patients during and after COVID-19. Our initial findings indicate that eosinophils are recruited to the lungs after SARS-CoV-2 infection in mice and that eosinophil-deficient mice may have increased lung viral titers early after infection. In keeping with this hypothesis, serum levels of eosinophil granule proteins (a marker of tissue eosinophilia) were increased during active SARS-CoV-2 infection in patients participating in a long-term follow-up study of COVID-19, at a time when eosinophil counts were depressed. These preliminary data suggest that eosinophils may have a protective role in early anti-viral host defense during SARS-CoV-2 infection in mice and that further studies are required to better understand the relative roles of eosinophils in protection and pathology to SARS-CoV-2 infection.

Funding for this study was provided in part by the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health.

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