MassIVE MSV000086925

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Dynamic multi-organ dysfunction in severe COVID-19 drives innate immune responses and tissue injury

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Description

Severe SARS-CoV-2 infection causes COVID-19. The host response to SARS-CoV-2 is poorly understood partly due to a lack of an animal model that recapitulates severe manifestations of human disease. Here we report a Syrian hamster model that develops a rapidly progressive lethal pulmonary disease that closely mimics human severe COVID-19. We evaluated host responses to infection using a multi-omics, multi-organ approach to define kinetic changes to the proteome, the phospho-proteome, and the transcriptome. These data revealed a robust antiviral response composed of both Type I and Type II interferon responses at the gene and protein levels. Both IFN and TNF-a responses were associated with peak viral replication at day 2 post-infection. These responses correlated to rapidly developing diffuse alveolar destruction and pneumonia that persisted in the absence of active viral infection. Extrapulmonary viral replication was detected in the heart and kidneys, which correlated with proteome and phospho-proteome remodeling in each organ. In addition to early antiviral responses, there was a significant and progressive increase in chemokines, monocyte, and neutrophil-associated molecules throughout the course of infection that peaked in the later time points. Together, our results provide a kinetic overview of multi-organ host responses to severe SARS-CoV-2 infection in vivo. [doi:10.25345/C5BN4P] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Corona Virus ; COVID-19 ; Tissue Injury ; Innate Immunity ; Proteomics ; Phosphoproteomics

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Principal Investigators:
(in alphabetical order) 		Norberto Gonzalez-Juarbe, J. Craig Venter Institute, USA
Submitting User: yayu
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