Host response to SARS-CoV-2: Insight from transcriptomic studies

Abstract

In the recent months, a number of transcriptomic studies have generated high-resolution data on the genes and pathways that are dysregulated in the patients infected with SARS-CoV-2 and enriched our understanding of the disease biology of this novel viral infection. The cumulative evidence collected from these data are considered in this article. Three motifs emerge with potential for future research and clinical translation. First, instead of a broad cytokine storm, one needs to interrogate the disease in terms of timing of specific cytokine up-regulation. Second, there is a subpopulation of immature or developing neutrophils in the patients with severe COVID-19 illness. This needs to be probed further for mechanistic insight and possible drug targets. Third, complement and coagulation cascades are significantly dysregulated in COVID-19, leading to the common clinical observation of a hypercoagulable state being associated with poor outcome. Interactions of these pathways with other immune-inflammatory pathways are important areas of future research. Finally, with rapid advances in relevant technologies in medicine (clinical transcriptomics, systems biology and artificial intelligence), we envisage deployment of these platforms in the clinical laboratory which shall benefit timely management of critical infectious illnesses such as COVID-19 and sepsis.