Abstract
The COVID-19 pandemic demands assimilation of all biomedical knowledge to decode mechanisms of pathogenesis. Despite the recent renaissance in neural networks, a platform for the real-time synthesis of the exponentially growing biomedical literature and deep omics insights is unavailable. Here, we present the nferX platform for dynamic inference from over 45 quadrillion possible conceptual associations from unstructured text, and triangulation with insights from single-cell RNA-sequencing, bulk RNA-seq and proteomics from diverse tissue types. A hypothesis-free profiling of ACE2 suggests tongue keratinocytes, olfactory epithelial cells, airway club cells and respiratory ciliated cells as potential reservoirs of the SARS-CoV-2 receptor. We find the gut as the putative hotspot of COVID-19, where a maturation correlated transcriptional signature is shared in small intestine enterocytes among coronavirus receptors (ACE2, DPP4, ANPEP). A holistic data science platform triangulating insights from structured and unstructured data holds potential for accelerating the generation of impactful biological insights and hypotheses.
Highlights
Since December 2019, the Severe Acute Respiratory Syndrome (SARS)-CoV-2 virus has been rapidly spreading across the globe
SARS, Middle East respiratory syndrome (MERS), and COVID-19 are all caused by Coronaviruses (CoV), deriving their name from the crown-like spike proteins protruding from the viral capsid surface
ACE2 has higher expression levels in multiple cell types of the Gastrointestinal (GI) tract compared to respiratory cells To systematically profile the transcriptional expression of ACE2 across tissues and cell types, we triangulated single cell RNAseq-based measurements with literature-derived signals to automatically delineate novel, emerging, and known expression patterns (Figure 2B; Table S1)
Summary
Since December 2019, the SARS-CoV-2 virus has been rapidly spreading across the globe. SARS, MERS, and COVID-19 are all caused by Coronaviruses (CoV), deriving their name from the crown-like spike proteins protruding from the viral capsid surface. Coronavirus infection is driven by the attachment of the viral spike protein to specific human cell-surface receptors: ACE2 for SARS-CoV-2 and SARS-CoV2–4, DPP4 for MERS-CoV5 and ANPEP for specific ɑ-coronaviruses[6]. In addition to these receptors, the protease activity of TMPRSS2 has been implicated in viral entry[7,8]
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