Transcriptomic similarities and differences in host response between SARS-CoV-2 and other viral infections

Summary: The pandemic 2019 novel coronavirus disease (COVID-19) shares certain clinical characteristics with other acute viral infections. We studied the whole-blood transcriptomic host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) using RNAseq from 24 healthy controls and...

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Main Authors: Simone A. Thair, Yudong D. He, Yehudit Hasin-Brumshtein, Suraj Sakaram, Rushika Pandya, Jiaying Toh, David Rawling, Melissa Remmel, Sabrina Coyle, George N. Dalekos, Ioannis Koutsodimitropoulos, Glykeria Vlachogianni, Eleni Gkeka, Eleni Karakike, Georgia Damoraki, Nikolaos Antonakos, Purvesh Khatri, Evangelos J. Giamarellos-Bourboulis, Timothy E. Sweeney
Format: Article
Language:English
Published: Elsevier 2021-01-01
Series:iScience
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Online Access:http://www.sciencedirect.com/science/article/pii/S2589004220311445
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Summary:Summary: The pandemic 2019 novel coronavirus disease (COVID-19) shares certain clinical characteristics with other acute viral infections. We studied the whole-blood transcriptomic host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) using RNAseq from 24 healthy controls and 62 prospectively enrolled patients with COVID-19. We then compared these data to non-COVID-19 viral infections, curated from 23 independent studies profiling 1,855 blood samples covering six viruses (influenza, respiratory syncytial virus (RSV), human rhinovirus (HRV), severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1), Ebola, dengue). We show gene expression changes in COVID-19 versus non-COVID-19 viral infections are highly correlated (r = 0.74, p < 0.001). However, we also found 416 genes specific to COVID-19. Inspection of top genes revealed dynamic immune evasion and counter host responses specific to COVID-19. Statistical deconvolution of cell proportions maps many cell type proportions concordantly shifting. Discordantly increased in COVID-19 were CD56bright natural killer cells and M2 macrophages. The concordant and discordant responses mapped out here provide a window to explore the pathophysiology of the host response to SARS-CoV-2.
ISSN:2589-0042