bioRxiv Science⌕ Search

bioRxiv · 10.1101/2023.11.03.565433

Virus-Host Interactions Predictor (VHIP): machine learning approach to resolve microbial virus-host interaction networks

Abstract

Viruses of microbes are ubiquitous biological entities that reprogram their hosts metabolisms during infection in order to produce viral progeny, impacting the ecology and evolution of microbiomes with broad implications for human and environmental health. Advances in genome sequencing have led to the discovery of millions of novel viruses and an appreciation for the great diversity of viruses on Earth. Yet, with knowledge of only "who is there?" we fall short in our ability to infer the impacts of viruses on microbes at population, community, and ecosystem-scales. To do this, we need a more explicit understanding "who do they infect?" Here, we developed a novel machine learning model (ML), Virus-Host Interaction Predictor (VHIP), to predict virus-host interactions (infection/non-infection) from input virus and host genomes. This ML model was trained and tested on a high-value manually curated set of 8849 virus-host pairs and their corresponding sequence data. The resulting dataset, Virus Host Range network (VHRnet), is core to VHIP functionality. Each data point that underlies the VHIP training and testing represents a lab-tested virus-host pair in VHRnet, from which features of coevolution were computed. VHIP departs from existing virus-host prediction models in its ability to predict multiple interactions rather than predicting a single most likely host or host clade. As a result, VHIP is the first virus-host range prediction tool able to reconstruct the complexity of virus-host networks in natural systems. VHIP has an 87.8% accuracy rate at predicting interactions between virus-host pairs at the species level and can be applied to novel viral and host population genomes reconstructed from metagenomic datasets. Through the reconstruction of complete virus-host networks from novel data, VHIP allows for the integration of multilayer network theory into microbial ecology and opens new opportunities to study ecological complexity in microbial systems. Author summaryThe ecology and evolution of microbial communities are deeply influenced by viruses. Metagenomics analysis, the non-targeted sequencing of community genomes, has led to the discovery of millions of novel viruses. Yet, through the sequencing process, only DNA sequences are recovered, begging the question: which microbial hosts do those novel viruses infect? To address this question, we developed a computational tool to allow researchers to predict virus-host interactions from such sequence data. The power of this tool is its use of a high-value, manually curated set of 8849 lab-verified virus-host pairs and their corresponding sequence data. For each pair, we computed signals of coevolution to use as the predictive features in a machine learning model designed to predict interactions between viruses and hosts. The resulting model, Virus-Host Interaction Predictor (VHIP), has an accuracy of 87.8% and can be applied to novel viral and host genomes reconstructed from metagenomic datasets. Because the model considers all possible virus-host pairs, it can resolve complete virus-host interaction networks and supports a new avenue to apply network thinking to viral ecology.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Bastien, G. E., Cable, R. N., Zaman, L., Batterbee, C., Wing, A. J., Duhaime, M. B.. 2023-11-05. Virus-Host Interactions Predictor (VHIP): machine learning approach to resolve microbial virus-host interaction networks. https://doi.org/10.1101/2023.11.03.565433

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Accelerating discovery and integration from RNA to Protein with R2T2P

Integrating transcriptomics and proteomics data remains an unmet challenge in the post-genomics era, discouraging researchers from pursuing integrative approaches to molecular biology research. Leveraging the power of translation profiling, we present RNA to Translation to Protein (R2T2P), a computational platform integrating genome-guided transcriptome assembly with identification of translation and proteins, including a tailored differential analysis framework and support for multiple reference transcriptomes. We applied R2T2P to investigate a cellular model of facioscapulohumeral muscular dystrophy (FSHD), where ectopic expression of the DUX4 retrogene in skeletal muscle triggers significant alterations in transcription and RNA metabolism. We uncovered hundreds of uncharacterized, highly overexpressed RNAs, including antisense and alternative transcripts, and quantified their contribution to translatome and proteome. Re-analysis of expression datasets from patient-derived myotubes and muscle biopsies validated this alternative transcriptome in FSHD patients, adding a reservoir of bona-fide novel molecular actors in a rare disease. Available at https://github.com/nfdata-omics/R2T2P/, R2T2P is a flexible and powerful workflow in modern integrative biology.

bioinformatics↗

MorphoANOVA: Dissecting Histology-Gene Expression Relationships in Spatial Transcriptomics

Spatial transcriptomics (ST) measures the expression of hundreds to thousands of genes within tissue architecture, often accompanied by histology images. However, it remains challenging to systematically characterize which genes exhibit associations with tissue morphology, whether these associations vary spatially, and which genes show additional spatial expression patterns beyond those captured by morphology. Here we introduce MorphoANOVA, a gene-wise statistical framework for characterizing morphology--expression relationships across genes measured by ST. Using nested spatially varying coefficient models and sequential ANOVA, MorphoANOVA assesses slide-wide associations with an H\&E-derived morphology feature, location-specific changes in these associations, and additional spatial variation after accounting for the selected feature. The resulting statistics enable gene prioritization and pathway enrichment analysis, while spatial component maps support the interpretation of individual genes. Simulations demonstrate MorphoANOVA's ability to distinguish the modeled components and recover their spatial patterns. Applications to human cortex and breast cancer identify biological programs associated with different morphology--expression patterns and reveal distinct relationships with cell composition. Across three HER2-positive breast cancer patients, invasive-cancer marker genes consistently exhibit stronger evidence of location-specific morphology associations. MorphoANOVA thus provides a framework for systematically interpreting spatial gene-expression patterns in relation to tissue morphology.

bioinformatics↗

Evaluation effects can rival reported concordance gains in cross-cancer survival prediction

Studies of cross-cancer learning for survival prediction from tumour omics have reported concordance gains of 0.020 and 0.045, but how such gains compare with evaluation effects remains unclear. We examined these effects across 13 TCGA cancers (5,761 patients, 1,526 disease-specific deaths), using five repeats of five-fold cross-validation and paired bootstrap intervals. When model selection did not use test data, our borrowing model gained 0.009 (95% interval 0.001 to 0.016) over its target-fitted reference when cancers received equal weight (post hoc). Random-effects pooling gave a gain of 0.002 (-0.002 to 0.006), with most weight assigned to cancers where the model made little use of the pretrained score. Choosing the fusion weight on test splits raised the apparent equal-weight gain to 0.017. We reimplemented a published method, VAECox, which showed no pretraining gain over random initialisation at the last or validation-selected training step. Choosing each network's best test step, as the published code does, raised concordance by 0.03 to 0.05 across the 13-cancer and ten-cancer overall-survival settings, but barely changed the difference between networks. In a constructed post hoc experiment, choosing the best test step only for the pretrained network changed the equal-weight mean difference from -0.004 to +0.045 (+0.035 to +0.054). Across seven multi-omics comparisons, estimates from single five-fold runs differed from their cancer's five-run mean by at least 0.02 in 11% to 42% of runs. Concordance was about 0.02 lower at held-out tissue source sites. Interpreting a reported gain therefore requires each model's selection rule, variation across repeated partitions, the weighting of cancers and the evaluation population.

bioinformatics↗