Equine papillomavirus type 2: An equine equivalent to human papillomavirus 16?

Sykora, Sabine; Jindra, Christoph; Hofer, Martin; Steinborn, Ralf; Brandt, Sabine

doi:10.1016/j.tvjl.2017.04.014

“…These may gradually progress to cancerous lesions like locally aggressive CIS and finally to invasive SCCs [5,6]. The EcPV2 genome has been shown to reside in up to 100% of early and late lesions in an episomal and/or integrated form [4,7,8]. In a subset of lesions, infection also appears to be productive, as evidenced by immunocapture PCR-mediated detection of virion-like structures [7].…”

Section: Introductionmentioning

confidence: 99%

Paving the way for more precise diagnosis of EcPV2-associated equine penile lesions

Ramsauer

¹

,

Wachoski-Dark

²

,

Fraefel

³

et al. 2019

Preprint

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Background There is growing evidence that equine papillomavirus type 2 (EcPV2) infection is causally associated with the development of equine genital squamous cell carcinomas (SCCs). Early stages of disease present clinically as plaques or wart-like lesions which can gradually progress to tumoural lesions. Histologically these lesions are inconsistently described as benign hyperplasia, papilloma, penile intraepithelial neoplasia (PIN), carcinoma in situ (CIS) or SCC. Guidelines for histological classification of early SCC precursor lesions are not precisely defined, leading to potential misdiagnosis. The aim of this study was to identify histologic criteria and diagnostic markers allowing for a more accurate diagnosis of EcPV2-associated equine penile lesions. Results A total of 61 archived equine penile lesions were histologically re-assessed and classified as benign hyperplasia, papilloma, CIS or SCC. From these, 19 representative lesions and adjacent normal skin were comparatively analysed for the presence of EcPV2 DNA and transcripts using PCR and RNA in situ hybridisation (RISH). All lesional samples were positive by EcPV2 PCR and RISH, while adjacent normal skin was negative. RISH analysis yielded signal distribution patterns that allowed distinction of early (hyperplasia, papilloma) from late stage lesions (CIS, SCC). Subsequently, the 19 lesions were further assessed for expression of p53, Ki67, MCM7 and MMP1 by immunohistochemistry (IHC). All four proteins were expressed in both normal and lesional tissue. However, p53 expression was up-regulated in basal keratinocyte layers of papillomas, CIS and SCCs, as well as in upper keratinocyte layers of CIS and SCCs. MCM7 expression was only up-regulated in upper proliferating keratinocyte layers of papillomas, CIS and SCCs. Conclusion This study proposes combining a refined histological protocol for analysis of equine penile lesions with PCR- and/or RISH based EcPV2-screening and p53/MCM7 IHC to more accurately determine the type of lesion. This may help to guide the choice of optimum treatment strategy, especially at early stages of disease.

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“…For oncologists, it is not necessarily apparent that cancers in a single anatomical location can be different clinical entities depending on the viral aetiology [19]. For comparative pathologists, it may be difficult to recognize that distantly related viruses can cause cancers in the same anatomical location by analogous but not homologous mechanisms [20]. Finally, as a significant side effect, the emphasis on cancer has potentially neglected many other clinical implications of the chronic viral infections, such as effects on fertility or even potential mutualistic effect [21].…”

Section: The Challenge Of Defining a Commonmentioning

confidence: 99%

Towards a multi-level and a multi-disciplinary approach to DNA oncovirus virulence

Alizon

¹

,

Bravo

²

,

Farrell

³

et al. 2019

Phil. Trans. R. Soc. B

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One out of 10 cancers is estimated to arise from infections by a handful of oncogenic viruses. These infectious cancers constitute an opportunity for primary prevention through immunization against the viral infection, for early screening through molecular detection of the infectious agent, and potentially for specific treatments, by targeting the virus as a marker of cancer cells. Accomplishing these objectives will require a detailed understanding of the natural history of infections, the mechanisms by which the viruses contribute to disease, the mutual adaptation of viruses and hosts, and the possible viral evolution in the absence and in the presence of the public health interventions conceived to target them. This issue showcases the current developments in experimental tissue-like and animal systems, mathematical models and evolutionary approaches to understand DNA oncoviruses. Our global aim is to provide proximate explanations to the present-day interface and interactions between virus and host, as well as ultimate explanations about the adaptive value of these interactions and about the evolutionary pathways that have led to the current malignant phenotype of oncoviral infections. This article is part of the theme issue ‘Silent cancer agents: multi-disciplinary modelling of human DNA oncoviruses’.

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“…In humans, diagnosis of penile precancerous lesions and invasive carcinomas is likewise challenging [11]. Given that human penile precursor lesions and SCCs closely resemble their equine counterpart [7,26], this study attempted to categorize EcPV2-associated equine penile lesions based on human data [9] and descriptions of equine disease [6,10,[23][24][25] in order to obtain well defined histological classes regardless of their clinical appearance.…”

Section: Proposal For Histological Classification Of Ecpv2-associatedmentioning

confidence: 99%

“…These may gradually progress to cancerous lesions like locally aggressive CIS and finally to invasive SCCs [5,6]. The EcPV2 genome has been shown to reside in up to 100% of early and late lesions in an episomal and integrated form [4,7,8]. In a subset of lesions, infection also appears to be productive, as evidenced by immunocapture PCR-mediated detection of virion-like structures [7].…”

Section: Introductionmentioning

confidence: 99%

“…The EcPV2 genome has been shown to reside in up to 100% of early and late lesions in an episomal and integrated form [4,7,8]. In a subset of lesions, infection also appears to be productive, as evidenced by immunocapture PCR-mediated detection of virion-like structures [7]. Importantly, EcPV2 transcribes its two oncogenes E6 and E7 at all stages of disease, which strengthens the evidence for an active involvement of this virus in progression of benign lesions to malignant neoplasms [4,7,8].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Paving the way for more precise diagnosis of EcPV2-associated equine penile lesions

Ramsauer

¹

,

Wachoski-Dark

²

,

Fraefel

³

et al. 2019

Preprint

0

View full text Add to dashboard Cite

Background There is growing evidence that equine papillomavirus type 2 (EcPV2) infection is causally associated with the development of equine genital squamous cell carcinomas (SCCs). Early stages of disease present clinically as plaques or wart-like lesions which can gradually progress to tumoural lesions. Histologically these lesions are inconsistently described as benign hyperplasia, papilloma, penile intraepithelial neoplasia (PIN), carcinoma in situ (CIS) or SCC. Guidelines for histological classification of early SCC precursor lesions are not precisely defined, leading to potential misdiagnosis. The aim of this study was to identify histologic criteria and diagnostic markers allowing for a more accurate diagnosis of EcPV2-associated equine penile lesions. Results A total of 61 archived equine penile lesions were histologically re-assessed and classified as benign hyperplasia, papilloma, CIS or SCC. From these, 19 representative lesions and adjacent normal skin were comparatively analysed for the presence of EcPV2 DNA and transcripts using PCR and RNA in situ hybridisation (RISH). All lesional samples were positive by EcPV2 PCR and RISH, while adjacent normal skin was negative. RISH analysis yielded signal distribution patterns that allowed distinction of early (hyperplasia, papilloma) from late stage lesions (CIS, SCC). Subsequently, the 19 lesions were further assessed for expression of p53, Ki67, MCM7 and MMP1 by immunohistochemistry (IHC). All four proteins were expressed in both normal and lesional tissue. However, p53 expression was up-regulated in basal keratinocyte layers of papillomas, CIS and SCCs, as well as in upper keratinocyte layers of CIS and SCCs. MCM7 expression was only up-regulated in upper proliferating keratinocyte layers of papillomas, CIS and SCCs. Conclusion This study proposes combining a refined histological protocol for analysis of equine penile lesions with PCR- and/or RISH based EcPV2-screening and p53/MCM7 IHC to more accurately determine the type of lesion. This may help to guide the choice of optimum treatment strategy, especially at early stages of disease.

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Equine papillomavirus type 2: An equine equivalent to human papillomavirus 16?

Cited by 35 publications

References 21 publications

Paving the way for more precise diagnosis of EcPV2-associated equine penile lesions

Paving the way for more precise diagnosis of EcPV2-associated equine penile lesions

Towards a multi-level and a multi-disciplinary approach to DNA oncovirus virulence

Paving the way for more precise diagnosis of EcPV2-associated equine penile lesions

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