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DeepViral: infectious disease phenotypes improve prediction of novel virus–host interactions

View ORCID ProfileWang Liu-Wei, View ORCID ProfileŞenay Kafkas, View ORCID ProfileJun Chen, View ORCID ProfileNicholas Dimonaco, View ORCID ProfileJesper Tegnér, View ORCID ProfileRobert Hoehndorf
doi: https://doi.org/10.1101/2020.04.22.055095
Wang Liu-Wei
1Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
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Şenay Kafkas
1Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
2Computational Bioscience Research Center, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
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Jun Chen
1Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
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Nicholas Dimonaco
4Institute of Biological, Environmental and Rural Sciences, Aberystwyth University, Aberystwyth, Wales, UK
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Jesper Tegnér
1Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
3Biological and Environmental Science and Engineering Division, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
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Robert Hoehndorf
1Computer, Electrical and Mathematical Sciences and Engineering Division, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
2Computational Bioscience Research Center, King Abdullah University of Science and Technology, Thuwal 23955, Saudi Arabia
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  • For correspondence: robert.hoehndorf@kaust.edu.sa
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Abstract

Motivation Infectious diseases from novel viruses have become a major public health concern. Rapid identification of virus–host interactions can reveal mechanistic insights into infectious diseases and shed light on potential treatments. Current computational prediction methods for novel viruses are based mainly on protein sequences. However, it is not clear to what extent other important features, such as the symptoms caused by the viruses, could contribute to a predictor. Disease phenotypes (i.e., signs and symptoms) are readily accessible from clinical diagnosis and we hypothesize that they may act as a potential proxy and an additional source of information for the underlying molecular interactions between the pathogens and hosts.

Results We developed DeepViral, a deep learning based method that predicts protein–protein interactions (PPI) between humans and viruses. Motivated by the potential utility of infectious disease phenotypes, we first embedded human proteins and viruses in a shared space using their associated phenotypes and functions, supported by formalized background knowledge from biomedical ontologies. By jointly learning from protein sequences and phenotype features, DeepViral significantly improves over existing sequence-based methods for intra- and inter-species PPI prediction. Lastly, we propose a novel experimental setup to realistically evaluate prediction methods for novel viruses.

Availability https://github.com/bio-ontology-research-group/DeepViral

Contact robert.hoehndorf{at}kaust.edu.sa

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted August 12, 2020.
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DeepViral: infectious disease phenotypes improve prediction of novel virus–host interactions
Wang Liu-Wei, Şenay Kafkas, Jun Chen, Nicholas Dimonaco, Jesper Tegnér, Robert Hoehndorf
bioRxiv 2020.04.22.055095; doi: https://doi.org/10.1101/2020.04.22.055095
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DeepViral: infectious disease phenotypes improve prediction of novel virus–host interactions
Wang Liu-Wei, Şenay Kafkas, Jun Chen, Nicholas Dimonaco, Jesper Tegnér, Robert Hoehndorf
bioRxiv 2020.04.22.055095; doi: https://doi.org/10.1101/2020.04.22.055095

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