Dataset Information

Predicting the global mammalian viral sharing network using phylogeography.

ABSTRACT: Understanding interspecific viral transmission is key to understanding viral ecology and evolution, disease spillover into humans, and the consequences of global change. Prior studies have uncovered macroecological drivers of viral sharing, but analyses have never attempted to predict viral sharing in a pan-mammalian context. Using a conservative modelling framework, we confirm that host phylogenetic similarity and geographic range overlap are strong, nonlinear predictors of viral sharing among species across the entire mammal class. Using these traits, we predict global viral sharing patterns of 4196 mammal species and show that our simulated network successfully predicts viral sharing and reservoir host status using internal validation and an external dataset. We predict high rates of mammalian viral sharing in the tropics, particularly among rodents and bats, and within- and between-order sharing differed geographically and taxonomically. Our results emphasize the importance of ecological and phylogenetic factors in shaping mammalian viral communities, and provide a robust, general model to predict viral host range and guide pathogen surveillance and conservation efforts.

SUBMITTER: Albery GF

PROVIDER: S-EPMC7210981 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Predicting the global mammalian viral sharing network using phylogeography.

Albery Gregory F GF Eskew Evan A EA Ross Noam N Olival Kevin J KJ

Nature communications 20200508 1

Understanding interspecific viral transmission is key to understanding viral ecology and evolution, disease spillover into humans, and the consequences of global change. Prior studies have uncovered macroecological drivers of viral sharing, but analyses have never attempted to predict viral sharing in a pan-mammalian context. Using a conservative modelling framework, we confirm that host phylogenetic similarity and geographic range overlap are strong, nonlinear predictors of viral sharing among ...[more]

PMID: 32385239

Similar Datasets

Project description:BackgroundEukaryotic gene regulation is a complex process comprising the dynamic interaction of enhancers and promoters in order to activate gene expression. In recent years, research in regulatory genomics has contributed to a better understanding of the characteristics of promoter elements and for most sequenced model organism genomes there exist comprehensive and reliable promoter annotations. For enhancers, however, a reliable description of their characteristics and location has so far proven to be elusive. With the development of high-throughput methods such as ChIP-seq, large amounts of data about epigenetic conditions have become available, and many existing methods use the information on chromatin accessibility or histone modifications to train classifiers in order to segment the genome into functional groups such as enhancers and promoters. However, these methods often do not consider prior biological knowledge about enhancers such as their diverse lengths or molecular structure.ResultsWe developed enhancer HMM (eHMM), a supervised hidden Markov model designed to learn the molecular structure of promoters and enhancers. Both consist of a central stretch of accessible DNA flanked by nucleosomes with distinct histone modification patterns. We evaluated the performance of eHMM within and across cell types and developmental stages and found that eHMM successfully predicts enhancers with high precision and recall comparable to state-of-the-art methods, and consistently outperforms those in terms of accuracy and resolution.ConclusionseHMM predicts active enhancers based on data from chromatin accessibility assays and a minimal set of histone modification ChIP-seq experiments. In comparison to other 'black box' methods its parameters are easy to interpret. eHMM can be used as a stand-alone tool for enhancer prediction without the need for additional training or a tuning of parameters. The high spatial precision of enhancer predictions gives valuable targets for potential knockout experiments or downstream analyses such as motif search.

Project description:BackgroundNetwork Component Analysis (NCA) has been used to deduce the activities of transcription factors (TFs) from gene expression data and the TF-gene binding relationship. However, the TF-gene interaction varies in different environmental conditions and tissues, but such information is rarely available and cannot be predicted simply by motif analysis. Thus, it is beneficial to identify key TF-gene interactions under the experimental condition based on transcriptome data. Such information would be useful in identifying key regulatory pathways and gene markers of TFs in further studies.ResultsWe developed an algorithm to trim network connectivity such that the important regulatory interactions between the TFs and the genes were retained and the regulatory signals were deduced. Theoretical studies demonstrated that the regulatory signals were accurately reconstructed even in the case where only three independent transcriptome datasets were available. At least 80% of the main target genes were correctly predicted in the extreme condition of high noise level and small number of datasets. Our algorithm was tested with transcriptome data taken from mice under rapamycin treatment. The initial network topology from the literature contains 70 TFs, 778 genes, and 1423 edges between the TFs and genes. Our method retained 1074 edges (i.e. 75% of the original edge number) and identified 17 TFs as being significantly perturbed under the experimental condition. Twelve of these TFs are involved in MAPK signaling or myeloid leukemia pathways defined in the KEGG database, or are known to physically interact with each other. Additionally, four of these TFs, which are Hif1a, Cebpb, Nfkb1, and Atf1, are known targets of rapamycin. Furthermore, the trimmed network was able to predict Eno1 as an important target of Hif1a; this key interaction could not be detected without trimming the regulatory network.ConclusionsThe advantage of our new algorithm, relative to the original NCA, is that our algorithm can identify the important TF-gene interactions. Identifying the important TF-gene interactions is crucial for understanding the roles of pleiotropic global regulators, such as p53. Also, our algorithm has been developed to overcome NCA's inability to analyze large networks where multiple TFs regulate a single gene. Thus, our algorithm extends the applicability of NCA to the realm of mammalian regulatory network analysis.

Dataset Information

Predicting the global mammalian viral sharing network using phylogeography.

Publications

Predicting the global mammalian viral sharing network using phylogeography.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets