Host Genetic Influence on Papillomavirus-Induced Tumors in the Horse

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A recent article was published on the Wiley Online library from the International Journal of Cancer that was titled, “Host genetic influence on papillomavirus-induced tumors in the horse.” You can purchase access to this article online. The research was sponsored by the Morris Animal Foundationand, the Harry M. Zweig Memorial Fund, and the Dorothy Russell Havemeyer Foundation, Inc.

Following is the abstract for this article.

Abstract

The common equine skin tumors known as sarcoids have been causally associated with infection by bovine papillomavirus (BPV). Additionally, there is evidence for host genetic susceptibility to sarcoids. We investigated the genetic basis of susceptibility to sarcoid tumors on a cohort of 82 affected horses and 270 controls genotyped on a genome-wide platform and two custom panels. A Genome Wide Association Study (GWAS) identified candidate regions on six chromosomes. Bayesian probability analysis of the same dataset verified only the regions on equine chromosomes (ECA) 20 and 22. Fine mapping using custom-produced SNP arrays for ECA20 and ECA22 regions identified two marker loci with high levels of significance: SNP BIEC2-530826 (map position 32,787,619) on ECA20 in an intron of the DQA1 gene in the Major Histocompatibility Complex (MHC) class II region (p=4.6e-06), and SNP BIEC2-589604 (map position 25,951,536) on ECA22 in a 200 kb region containing four candidate genes: PROCR, EDEM2, EIF6 and MMP24 (p =2.14e-06). The marker loci yielded odds ratios of 5.05 and 4.02 for ECA20 and ECA22, respectively. Associations between genetic MHC class II variants and papillomavirus-induced tumors have been reported for human papillomavirus and cottontail rabbit papillomavirus infections. This suggests a common mechanism for susceptibility to tumor progression that may involve subversion of the host immune response. This study also identified a genomic region other than MHC that influenced papillomavirus-induced tumor development in the studied population.

Authors

Wlizabeth A. Staiger, Department of Animal Science, Cornell University, Ithaca, NY; Chia T. Tseng, Donald Miller, Jennifer M. Cassano, and Douglas F. Antczak, Baker Institute for Animal Health, Cornell University, Ithaca, NY; Lubna Nasir, MRC-University of Glasgow Centre for Virus Research, Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, UK; Dorian Garrick, Department of Animal Science, Iowa State University, Ames, IA; and Samantha A. Brooks, Department of Animal Science, University of Florida, Gainesville, FL.