Profiling cytokine storm in COVID-19 patients by metatranscriptomic sequencing

SARS-CoV-2 / COVID-19 pathogenesis is inextricably linked to immune system dysfunction. Hypercytokinemia (or “cytokine storm”) is a hyperinflammatory response that can lead to acute respiratory distress syndrome (ARDS) and other systemic complications in COVID-19 patients. To learn more about the immune signatures present in the respiratory tract following SARS-CoV-2 infection, Zhou et al. performed metatranscriptomic sequencing and functional analysis using bronchoalveolar lavage fluid (BALF) samples from healthy subjects and from patients with COVID-19 or community-acquired pneumonia (1). The authors found increased expression of multiple proinflammatory genes, especially chemokines (with CXCL17 consistently noted) and their receptors, in the COVID-19 samples. In addition, there was evidence of a strong interferon (IFN) response with at least 83 IFN-stimulated genes (ISGs) being upregulated. Significantly, genes mediating neutrophil (e.g., CXCL8) and monocyte (i.e., CCL2, CCL7) recruitment were overexpressed, an intriguing observation as these cells are in the alveoli of patients with ARDS. This also agrees with clinical findings that an elevated neutrophil:lymphocyte ratio is an indicator of aggressive disease. Finally, the authors report the downregulation of several neuron function-related pathways in the COVID-19 samples, which may offer important clues as to how this virus impacts the nervous system. In conclusion, this work demonstrates that SARS-CoV-2 corrupts the transcriptional profiles of innate immune cells in the lung, and establishes a framework for more specific mechanistic studies.

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Reference:

1. Zhou et al. Cell Host & Microbe (2020).