Association between equine leucocyte antigens (ELA) and equine sarcoid tumors in the population of Swedish Halfbreds and some of their families

Broström, Hans; Fahlbrink, E; Dubath, M. L.; Lazàry, S.

doi:10.1016/0165-2427(88)90109-2

Cited by 55 publications

(44 citation statements)

References 24 publications

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“…Ragland et al (1966), postulating on the virus aetiology of the disease, described an outbreak of sarcoids in a small group of horses and Reid et al (1994) estimated an incidence of 0?6 cases per 100 animal-years in a population of donkeys. Similarly, there have been descriptions of the disease occurring within particular breeds and bloodlines associated with equine leucocyte antigens (James, 1968;Lazary et al, 1985;Meredith et al, 1986;Angelos et al, 1988;Brostrom et al, 1988). Risk factors remain equivocal, although MHC type, age and sex are emerging as worthy of greater scrutiny.…”

Section: Epidemiologymentioning

confidence: 99%

“…These findings were the first to suggest an association between predisposition to sarcoids and particular MHC haplotypes (Meredith et al, 1986) and were later confirmed by subsequent studies. It was found that the W13 haplotype is associated strongly with sarcoids in Swedish halfbreds (Brostrom et al, 1988) and Swiss Warmbloods (Gerber et al, 1988). A further Swedish study showed that there is an association between increased recurrence of sarcoids following surgery with the W13 haplotype and association between early onset of sarcoids and the A5 haplotype (Brostrom, 1995).…”

Section: Other Factors Involved In Sarcoid Developmentmentioning

confidence: 99%

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Association of bovine papillomavirus with the equine sarcoid

Chambers

Ellsmore

O’Brien

et al. 2003

Journal of General Virology

186

180

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The equine sarcoid, a locally aggressive, fibroblastic skin tumour, is the most common dermatological neoplasm reported in horses; there is no consistently effective therapy. It is widely accepted that bovine papillomavirus (BPV) types 1 and 2 are associated with the pathogenesis of sarcoid disease. Most sarcoids appear to contain detectable viral DNA and RNA and are also known to express the BPV types 1 and 2 major transforming protein, E5, but appear not to produce infectious virions. While the mode of transmission of infection has not been elucidated, viral gene expression, in particular of E5, may contribute to virus persistence and disease pathogenesis by downregulating MHC class I expression. Here, the pathology and epidemiology of the sarcoid and its association with BPV is reviewed; the transforming functions of the BPV oncoproteins and their possible role in sarcoid pathogenesis are discussed; and the practical implications of BPV infection for diagnostic and therapeutic purposes are considered.

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Section: Epidemiologymentioning

confidence: 99%

Section: Other Factors Involved In Sarcoid Developmentmentioning

confidence: 99%

Association of bovine papillomavirus with the equine sarcoid

Chambers

Ellsmore

O’Brien

et al. 2003

Journal of General Virology

186

180

View full text Add to dashboard Cite

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“…Evidence for a genetic basis of ES as an important intrinsic factor includes family- (Ragland et al 1966;James 1968;Stannard 1978) and breed-predispositions (Angelos et al 1988;Mohammed et al 1992), associations of ES with certain equine leukocyte antigen alleles (Meredith et al 1986;Brostr€ om et al 1988;Lazary et al 1994) and with other genomic loci (Jandova et al 2012). Furthermore, a recent segregation analysis of ES disease in a large sample of the FranchesMontagnes (FM) horse population revealed an estimated heritability of up to 21% (Christen et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Clinical course of sarcoids in 61 Franches-Montagnes horses over a 5–7 year period

Berruex

Gerber

Wohlfender

et al. 2016

Veterinary Quarterly

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Background: The progression of equine sarcoids (ES) is notoriously unpredictable. Making a choice for the appropriate treatment is challenging when dealing with milder manifestations of ES. Objective: The aim of this study was to investigate the clinical course of ES in young horses. Animals and methods: A cohort of 61 ES-affected three-year-old Franches-Montagnes horses and a breed-, age-and geographically matched control group of 75 ES-free peers were examined twice over a period of 5À7 years. Owners and caretakers were queried, using a standardized questionnaire. Results: More than half of the 38/61 (62%) horses that were ES-affected at the age of three, had become ES-free at the time of follow-up. In 29 of 38 horses, representing 48% of the entire study population, ES lesions had spontaneously disappeared without therapy. When differentiating the clinical types of ES lesions, occult ES underwent complete spontaneous regression in 65% (11/17), while verrucous lesions regressed spontaneously in 32% (9/28). None of the evaluated intrinsic or environmental factors showed a significant effect on the risk for development, regression or exacerbation of ES disease. Conclusions: Our results document a surprisingly high rate of spontaneous ES regression for young horses affected with milder manifestations of ES disease. These findings justify a 'waitand-see' approach in selected cases of occult and verrucous ES, provided that all lesions are closely monitored. Furthermore, results of this study should also be considered when critically assessing treatment effects of therapies directed against ES, especially in the context of uncontrolled studies.

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“…The differences in sarcoid incidence between breeds suggests a genetic basis for resistance or susceptibility, and early studies conducted using serological assays demonstrated association between sarcoid occurrence and alleles of the equine Major Histocompatibility Complex (MHC) . In those studies the MHC class I antigen(s) of the Equine Leukocyte Antigen (ELA) A3 haplotype was associated with sarcoid incidence, and a stronger association was suggested with equine MHC class II alleles often linked to the same ELA‐A3 haplotype .…”

mentioning

confidence: 99%

Host genetic influence on papillomavirus‐induced tumors in the horse

Staiger

Tseng

Miller

et al. 2016

Intl Journal of Cancer

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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 5 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 5 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.

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Association between equine leucocyte antigens (ELA) and equine sarcoid tumors in the population of Swedish Halfbreds and some of their families

Cited by 55 publications

References 24 publications

Association of bovine papillomavirus with the equine sarcoid

Association of bovine papillomavirus with the equine sarcoid

Clinical course of sarcoids in 61 Franches-Montagnes horses over a 5–7 year period

Host genetic influence on papillomavirus‐induced tumors in the horse

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