Knowledge synthesis of 100 million biomedical documents augments the deep expression profiling of coronavirus receptors
- nference, United States
- nference, India
- Janssen, United States
- nference, Canada
- Cited 11
- Views 2,196
- Annotations
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 45 quadrillion+ possible conceptual associations from unstructured text and triangulation with insights from Single Cell RNA-sequencing, bulk RNAseq 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.
Article and author information
Author details
Dariusz K Murakowski
Venky Soundararajan
Funding
No external funding was received for this work.
Reviewing Editor
- Mone Zaidi, Icahn School of Medicine at Mount Sinai, United States
Publication history
- Received: April 18, 2020
- Accepted: May 27, 2020
- Accepted Manuscript published: May 28, 2020 (version 1)
- Version of Record published: July 20, 2020 (version 2)
Copyright
© 2020, Venkatakrishnan et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 2,196
- Page views
-
- 371
- Downloads
-
- 11
- Citations
Article citation count generated by polling the highest count across the following sources: PubMed Central, Crossref, Scopus.
Download links
Downloads (link to download the article as PDF)
Download citations (links to download the citations from this article in formats compatible with various reference manager tools)
Open citations (links to open the citations from this article in various online reference manager services)
Further reading
-
eLife has published the following articles on SARS-CoV-2 and COVID-19.
-
- Medicine
Obesity and diabetes are established comorbidities for COVID-19. Adipose tissue demonstrates high expression of ACE2 which SARS- CoV-2 exploits to enter host cells. This makes adipose tissue a reservoir for SARS-CoV-2 viruses and thus increases the integral viral load. Acute viral infection results in ACE2 downregulation. This relative deficiency can lead to disturbances in other systems controlled by ACE2, including the renin-angiotensin system. This will be further increased in the case of pre-conditions with already compromised functioning of these systems, such as in patients with obesity and diabetes. Here, we propose that interactions of virally-induced ACE2 deficiency with obesity and/or diabetes leads to a synergistic further impairment of endothelial and gut barrier function. The appearance of bacteria and/or their products in the lungs of obese and diabetic patients promotes interactions between viral and bacterial pathogens, resulting in a more severe lung injury in COVID-19.
