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Genome‐wide association study for host genetic factors associated with equine herpesvirus type‐1 induced myeloencephalopathy
Author(s) -
Dunuwille Wangisa M. B.,
YousefiMashouf Navid,
Balasuriya Udeni B. R.,
Pusterla Nicola,
Bailey Ernest
Publication year - 2020
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/evj.13261
Subject(s) - biology , genome wide association study , single nucleotide polymorphism , genetics , genetic association , haplotype , snp , genetic variation , gene , genotype
Background Equid herpesvirus (EHV‐1) infections in horses can lead to equine herpesvirus myeloencephalopathy (EHM), characterised by neurological clinical signs. The sporadic occurrence of the disease in horse herds suggests a host genetic component. A recent study reported an association between the occurrence of EHM and genetic markers on horse chromosome 6 (ECA6). Objectives To investigate the association of EHM with genetic host factors, especially with reference to the association reported for ECA6. Study design Genome‐wide association study (GWAS) was conducted based on 94 horses that had EHV‐1 infections and comparing the 27 developing clinical EHM to the 67 which did not. Methods DNA samples were tested from 94 horses for 382,529 single nucleotide polymorphisms (SNPs) with the Affymetrix Axiom 670K SNP array to identify possible associations with EHM. The data analysis included tests for basic, additive, dominant and recessive modes of inheritance, haplotype associations and runs of homozygosity (ROH). Results Results from this study did not identify significant SNPs, haplotypes or ROH associations with the development of EHM following EHV‐1 infections and excluded the involvement of a recessive genetic factor in the susceptibility to develop EHM. Main limitations Sample size and complex phenotype. Conclusions The results exclude the involvement of a recessive genetic factor in the susceptibility to develop clinically apparent EHM but do not have the power to exclude the involvement of other, complex host genetic factors. Furthermore, there was no association between development of EHM and genes on equine chromosome 6, as previously reported.