TY - JOUR
T1 - eDiVA-Classification and prioritization of pathogenic variants for clinical diagnostics
AU - Bosio, Mattia
AU - Drechsel, Oliver
AU - Rahman, Rubayte
AU - Muyas, Francesc
AU - Rabionet, Raquel
AU - Bezdan, Daniela
AU - Domenech Salgado, Laura
AU - Hor, Hyun
AU - Schott, Jean-Jacques
AU - Munell Casadesus, Francina
AU - Colobrán Oriol, Roger
AU - Macaya Ruiz, Alfons
AU - Estivill, Xavier
AU - Ossowski, Stephan
PY - 2019
Y1 - 2019
N2 - Mendelian diseases have shown to be an and efficient model for connecting genotypes to phenotypes and for elucidating the function of genes. Whole-exome sequencing (WES) accelerated the study of rare Mendelian diseases in families, allowing for directly pinpointing rare causal mutations in genic regions without the need for linkage analysis. However, the low diagnostic rates of 20-30% reported for multiple WES disease studies point to the need for improved variant pathogenicity classification and causal variant prioritization methods. Here, we present the exome Disease Variant Analysis (eDiVA; http://ediva.crg.eu), an automated computational framework for identification of causal genetic variants (coding/splicing single-nucleotide variants and small insertions and deletions) for rare diseases using WES of families or parent-child trios. eDiVA combines next-generation sequencing data analysis, comprehensive functional annotation, and causal variant prioritization optimized for familial genetic disease studies. eDiVA features a machine learning-based variant pathogenicity predictor combining various genomic and evolutionary signatures. Clinical information, such as disease phenotype or mode of inheritance, is incorporated to improve the precision of the prioritization algorithm. Benchmarking against state-of-the-art competitors demonstrates that eDiVA consistently performed as a good or better than existing approach in terms of detection rate and precision. Moreover, we applied eDiVA to several familial disease cases to demonstrate its clinical applicability.
AB - Mendelian diseases have shown to be an and efficient model for connecting genotypes to phenotypes and for elucidating the function of genes. Whole-exome sequencing (WES) accelerated the study of rare Mendelian diseases in families, allowing for directly pinpointing rare causal mutations in genic regions without the need for linkage analysis. However, the low diagnostic rates of 20-30% reported for multiple WES disease studies point to the need for improved variant pathogenicity classification and causal variant prioritization methods. Here, we present the exome Disease Variant Analysis (eDiVA; http://ediva.crg.eu), an automated computational framework for identification of causal genetic variants (coding/splicing single-nucleotide variants and small insertions and deletions) for rare diseases using WES of families or parent-child trios. eDiVA combines next-generation sequencing data analysis, comprehensive functional annotation, and causal variant prioritization optimized for familial genetic disease studies. eDiVA features a machine learning-based variant pathogenicity predictor combining various genomic and evolutionary signatures. Clinical information, such as disease phenotype or mode of inheritance, is incorporated to improve the precision of the prioritization algorithm. Benchmarking against state-of-the-art competitors demonstrates that eDiVA consistently performed as a good or better than existing approach in terms of detection rate and precision. Moreover, we applied eDiVA to several familial disease cases to demonstrate its clinical applicability.
KW - Disease variant prioritization
KW - Machine learning
KW - NGS diagnostics
KW - Rare genetic disease
KW - Whole-exome sequencing
UR - https://www.scopus.com/pages/publications/85069644655
U2 - 10.1002/humu.23772
DO - 10.1002/humu.23772
M3 - Article
C2 - 31026367
SN - 1098-1004
VL - 40
SP - 865
EP - 878
JO - Human Mutation (Print)
JF - Human Mutation (Print)
IS - 7
ER -