Frequent detection of papillomavirus DNA in clinically normal skin of cats infected and noninfected with feline immunodeficiency virus

Munday, John S.; Witham, Adrian I

doi:10.1111/j.1365-3164.2009.00811.x

Cited by 41 publications

(39 citation statements)

References 18 publications

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“…PV DNA was amplified from 50% of the SCCs in the present study. However, as PVs can asymptomatically infect feline skin, 28 the detection of PV DNA within a cutaneous SCC does not prove that the virus influenced neoplasm development. As has been reported, 22 PV DNA was detected in the present study more frequently in SCCs from UV-protected areas than in SCCs from UV-exposed skin.…”

Section: Discussionmentioning

confidence: 99%

Loss of Retinoblastoma Protein, But Not p53, Is Associated With the Presence of Papillomaviral DNA in Feline Viral Plaques, Bowenoid In Situ Carcinomas, and Squamous Cell Carcinomas

Munday

Aberdein

2011

Vet Pathol

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Although papillomaviral (PV) DNA is frequently present in feline cutaneous squamous cell carcinomas (SCCs), a causative association cannot be proven. Oncogenic human PVs cause neoplastic transformation by inhibiting retinoblastoma (pRb) and p53 activity. Therefore, absence of pRb and p53 immunostaining, along with increased p16 immunostaining, indicates a PV cause in some human SCCs. If PVs cause cutaneous feline SCCs, it was hypothesized that a similar immunohistochemistry profile, along with PV DNA, would be detectable. This was investigated using 5 feline viral plaques, 10 Bowenoid in situ carcinomas, 19 SCCs from ultraviolet-exposed (UV-exposed) skin, and 11 SCCs from UV-protected skin. Papillomaviral DNA was amplified by polymerase chain reaction from 30 of 45 lesions. Reduced pRb immunostaining was present in 26 of 45; increased p16 immunostaining was in 30; and p53 immunostaining was in 19. Both reduced pRb immunostaining and increased p16 immunostaining were more frequent in lesions containing PV DNA. In contrast, no association was observed between p53 immunostaining and the presence of PV DNA. SCCs from UV-protected skin more frequently contained PV DNA, reduced pRb, and increased p16 than UV-exposed SCCs. UV exposure was not associated with p53 immunostaining within the SCCs. These results suggest that feline PVs alter cell regulation by degrading pRb. Unlike oncogenic human PVs, there was no evidence that feline PVs degrade p53. These results provide further evidence that PVs may cause feline cutaneous SCCs, especially those in UV-protected skin, and they suggest a possible mechanism of this oncogenic action.

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Section: Discussionmentioning

confidence: 99%

Loss of Retinoblastoma Protein, But Not p53, Is Associated With the Presence of Papillomaviral DNA in Feline Viral Plaques, Bowenoid In Situ Carcinomas, and Squamous Cell Carcinomas

Munday

Aberdein

2011

Vet Pathol

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“…FcaPV-2 is thought to cause premalignant skin lesions including viral plaques and Bowenoid in situ carcinomas, as these lesions frequently contain FcaPV-2 DNA and cytopathic changes consistent with papillomavirus replication (Munday & Peters-Kennedy, 2010;Munday et al, 2007). Additionally, FcaPV-2 DNA has been found in skin swabs from normal cats, suggesting that subclinical infections may be common (Munday & Witham, 2010).…”

Section: Introductionmentioning

confidence: 99%

Frequent detection of transcriptionally active Felis catus papillomavirus 2 in feline cutaneous squamous cell carcinomas

Munday

Dittmer

2016

Journal of General Virology

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Felis catus papillomavirus 2 (FcaPV-2) causes premalignant skin lesions in cats and has also been found in a proportion of cutaneous squamous cell carcinomas (SCCs) -a common and potentially fatal cancer of cats. Whilst this could suggest a role of the virus in cancer development, FcaPV-2 has also been detected in skin swabs of normal cats, making it difficult to discern whether the papillomavirus is causing the cancer or merely an 'innocent bystander'. To distinguish between these two possibilities, real-time PCR was used to determine the viral copy number and the transcriptional activity of FcaPV-2 infections present in 70 formalin-fixed paraffin-embedded skin lesions including 10 papillomavirus-induced premalignant lesions and 60 SCCs. FcaPV-2 gene expression was found in 21 of 60 (35 %) SCCs, all 10 premalignant lesions and none of 10 normal skin samples. The results showed two distinct subsets of SCCs. The majority of the SCCs had low copy numbers of FcaPV-2 DNA (mean of 17 copies per copy of reference gene DNA) and no FcaPV-2 gene expression, suggesting the virus was an incidental finding. In contrast, 20 SCCs had detectable FcaPV-2 E6/E7 gene expression and very high copy numbers of FcaPV-2 DNA, with a mean of 32 930 copies per copy of reference gene DNA. The relative quantity of E6/E7 gene expression and the viral copy number in this group were similar to those found in the papillomavirus-induced premalignant lesions, suggesting that FcaPV-2 may play a role in the development of a subset of feline cutaneous SCCs.

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“…Asymptomatic PV infections are common in many species, 2 and more than half of cats are asymptomatically infected by Feline papillomavirus type 2 (FDPV-2). 15 Most PVs appear to be species-specific, 8 and recent investigations of equine sarcoids, a neoplasm that shares many features with feline sarcoids, 9 revealed that the causative PV is often present on equine skin. 3,16 Therefore, it was hypothesized that FeSarPV, frequently and asymptomatically, infects cats but rarely causes disease.…”

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confidence: 99%

“…Second, asymptomatic PV infection of feline skin is common. 15 Consensus primers may have amplified DNA from PVs other than FeSarPV making subsequent sequencing necessary. Additional sequencing was avoided in the present study by using specific primers.…”

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confidence: 99%

The Same Papillomavirus is Present in Feline Sarcoids from North America and New Zealand but Not in Any Non-Sarcoid Feline Samples

2010

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Abstract. Feline sarcoids are uncommon dermal neoplasms that are associated with papillomavirus (PV) infection. A single PV type, designated feline sarcoid-associated PV (FeSarPV), was detected in 9 feline sarcoids from North America. As FeSarPV has only been detected within feline sarcoids, the epidemiology of the infection remains unknown. The present study used polymerase chain reaction (PCR) to investigate whether this PV is also present within sarcoids from New Zealand cats. Additionally, as PVs are often host-specific, it was hypothesized that FeSarPV may often asymptomatically infect cats but rarely cause disease. To test this hypothesis, specific PCR primers were designed to investigate the presence of FeSarPV DNA within 120 samples from the skin and mouth of cats without sarcoids. Feline sarcoids from both New Zealand and North America contained FeSarPV DNA sequences. However, FeSarPV DNA was not detected within any non-sarcoid feline sample. To the authors' knowledge, this is the first time that FeSarPV has been reported in a country outside North America. As FeSarPV does not asymptomatically infect cats, feline sarcoids are likely due to cross-species infection. Although the reservoir host of FeSarPV is unknown, the host is present and has contact with cats, in both New Zealand and North America.

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Frequent detection of papillomavirus DNA in clinically normal skin of cats infected and noninfected with feline immunodeficiency virus

Cited by 41 publications

References 18 publications

Loss of Retinoblastoma Protein, But Not p53, Is Associated With the Presence of Papillomaviral DNA in Feline Viral Plaques, Bowenoid In Situ Carcinomas, and Squamous Cell Carcinomas

Loss of Retinoblastoma Protein, But Not p53, Is Associated With the Presence of Papillomaviral DNA in Feline Viral Plaques, Bowenoid In Situ Carcinomas, and Squamous Cell Carcinomas

Frequent detection of transcriptionally active Felis catus papillomavirus 2 in feline cutaneous squamous cell carcinomas

The Same Papillomavirus is Present in Feline Sarcoids from North America and New Zealand but Not in Any Non-Sarcoid Feline Samples

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