Abstract
The reason why most individuals with COVID-19 have relatively limited symptoms while other develop respiratory distress with life-threatening complications remains unknown. Increasing evidence suggests that COVID-19 associated adverse outcomes mainly rely on dysregulated immunity. Here, we compared transcriptomic profiles of blood cells from 103 patients with different severity levels of COVID-19 with that of 27 healthy and 22 influenza-infected individuals. Data provided a complete overview of SARS-CoV-2-induced immune signature, including a dramatic defect in IFN responses, a reduction of toxicity-related molecules in NK cells, an increased degranulation of neutrophils, a dysregulation of T cells, a dramatic increase in B cell function and immunoglobulin production, as well as an important over-expression of genes involved in metabolism and cell cycle in patients infected with SARS-CoV-2 compared to those infected with influenza viruses. These features also differed according to COVID-19 severity. Overall and specific gene expression patterns across groups can be visualized on an interactive website (https://bix.unil.ch/covid/). Collectively, these transcriptomic host responses to SARS-CoV-2 infection are discussed in the context of current studies, thereby improving our understanding of COVID-19 pathogenesis and shaping the severity level of COVID-19.
Highlights
Coronaviruses (CoV) are enveloped single-stranded positive-sense RNA viruses surrounded by spike glycoproteins shaping the typical “corona-like” appearance [1]
Characteristics of Patients Infected With Severe acute respiratory virus (SARS)-CoV-2 and Influenza Viruses
Blood gene-expression was measured in 103 patients infected with SARS-CoV-2 and compared to that of 22 patients infected with Influenza A or B (INFL) as well as 27 non-infected, healthy individuals (HLTY) COVID-19 patients were stratified according to the level of respiratory failure; 23 did not require oxygen support (“OXY0”), 40 received oxygen but no mechanical ventilation (“OXY1”) and 40 required mechanical ventilation (“TUBE”)
Summary
Coronaviruses (CoV) are enveloped single-stranded positive-sense RNA viruses surrounded by spike glycoproteins shaping the typical “corona-like” appearance [1]. Signal transduction by PRR subsequently leads to the induction of transcription factors such as interferon regulatory factors (IRFs) and nuclear factor k B (NF-k B), thereby inducing the synthesis and secretion of pro-inflammatory cytokines such as Type I and III interferons (IFNs), as well as the production of chemokines inducing adaptive immunity Both type I and III IFNs induce the expression of interferon stimulated genes (ISGs), which restrict and limit viral spread and stimulate the adaptive immune responses [5, 6], resulting in the generation of viral peptide-specific T cells [7, 8] and the production of viralspecific antibodies [9,10,11]
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