Spike protein multiorgan tropism suppressed by antibodies targeting SARS-CoV-2

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Molly Brady
Conor McQuaid
Alexander Solorzano
Angelique Johnson
Abigail Combs
Chethana Venkatraman
Akib Rahman
Hannah Leyva
Wing-Chi Edmund Kwok
Ronald W. Wood
Rashid Deane
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[1] University of Rochester,Department of Neuroscience, Del Monte Institute of Neuroscience
[2] University of Rochester,Department of Imaging Sciences
[3] University of Rochester,Departments of Obstetrics and Gynecology
[4] University of Rochester,Department of Urology
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While there is SARS-CoV-2 multiorgan tropism in severely infected COVID-19 patients, it’s unclear if this occurs in healthy young individuals. In addition, for antibodies that target the spike protein (SP), it’s unclear if these reduce SARS-CoV-2/SP multiorgan tropism equally. We used fluorescently labeled SP-NIRF to study viral behavior, using an in vivo dynamic imaging system and ex in vivo tissue analysis, in young mice. We found a SP body-wide biodistribution followed by a slow regional elimination, except for the liver, which showed an accumulation. SP uptake was highest for the lungs, and this was followed by kidney, heart and liver, but, unlike the choroid plexus, it was not detected in the brain parenchyma or CSF. Thus, the brain vascular barriers were effective in restricting the entry of SP into brain parenchyma in young healthy mice. While both anti-ACE2 and anti-SP antibodies suppressed SP biodistribution and organ uptake, anti-SP antibody was more effective. By extension, our data support the efficacy of these antibodies on SARS-CoV-2 multiorgan tropism, which could determine COVID-19 organ-specific outcomes.
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