GUIDELINE for Feline viral papillomatosis

The feline viral papillomatosis guidelines were first published in J Feline Med Surg 2013; 15: 560-562. This recent update has been compiled by Herman Egberink and ABCD colleagues with valuable input from Ralf Müller, Medizinische Kleintierklinik, Dermatologie und Allergologie, Ludwig-Maximilians-Universität, München, Germany.

Key points

• Papillomaviruses (PVs) are epitheliotropic and cause infections in humans and many different animal species, including fish.
• PV infections are associated with a variety of skin lesions and neoplasia but the virus can also be found in normal skin.
• Cats most likely become infected through lesions or abrasions of the skin.
• Besides cat-specific PVs, DNA sequences most closely related to human and bovine PVs have been detected in feline skin lesions.
• Diagnosis is supported by the histological detection of PV-induced cell changes and intralesional detection of viral antigen by immunostaining or DNA by in situ hybridization.
• There is no specific treatment for PV-induced skin lesions. Spontaneous regression commonly occurs.
• In case of invasive squamous cell carcinoma (ISCC), complete excision should be considered if possible.

Agent properties

Papillomaviruses (PVs) are small viruses containing circular double-stranded DNA and belong to the family Papillomaviridae (Fig. 1).

Fig. 1. Papilloma virions

The genome contains early (E) genes encoding several E proteins and two late (L) genes. Some of the E proteins play roles in viral transcription and replication. The E6 and E7 proteins are oncogenes that interfere with cell regulation. The L genes encode two structural proteins, L1 and L2, that form the capsid during virus assembly. In human PV-induced neoplasms, the viral DNA is integrated in the host-cell DNA. However, in papillomas (warts) the viral DNA is not integrated and persists as an autonomously replicating episome. Viral DNA integration also appears to be uncommon within PV-induced neoplasms in animals (MacLachlan et al., 2016). However, genomic integration and expression of feline PV oncogenes were shown in feline Merkel cell carcinoma (MCC) in cats (Ito et al., 2023).

Two subfamilies of PVs are recognized: firstpapillomavirinae (containing 52 genera and several hundred species) and secondpapillomavirinae (currently one genus). The conserved L1 gene is used for the classification of PVs. If two PVs have < 90% sequence similarity in the L gene, they are considered to be different types, and if < 60% similarity, to be within different genera (de Villiers et al., 2004; Bernard et al., 2010).In general, PVs are species-specific with tropism for mucosal and cutaneous epithelia and a preference for specific locations on the body (Doorbar, 2005; Doorbar et al., 2012). The majority of PVs cause asymptomatic or harmless infections, but some PV types can induce neoplasia. In each host, different PV types exist, as is true for cats (Munday and Thomson, 2021; Munday et al., 2017d). Presently, eight different PV types with complete genome sequences have been detected in cats, seven feline PVs (papillomaviruses 1-7; FcaPV1-7) and bovine PV14, which is a bovine-specific PV (BPV) found in cats with sarcoids. The feline PVs were previously designated as Felis domesticus PVs (FdPVs), but a more correct taxonomic name, Felis catus PVs (FcaPVs), has been proposed (Munday et al., 2013a). The feline PVs are classified within 3 genera: Lambdapapillomavirus (FcaPV1), Dyothetapapillomavirus (FcaPV2) and the Taupapillomavirus genus (FcaPV 3-7) (Munday et al., 2023). The BPV is an exception to the rule that PVs are highly species-specific (Munday and Thomson, 2021). A novel FcaPV type was suggested in a cat with a cutaneous papilloma, based on a low level of sequence similarity with known FcaPVs (Munday et al., 2022b) and another putative novel FcaPV type was determined in a feline osteoinductive squamous cell carcinoma (Munday et al., 2024).

Epidemiology

Papillomaviruses have been detected in several animal species and in man as a cause of cutaneous lesions (Munday and Kiupel, 2010). Although the viruses tend to be species-specific, sequences related to bovine and human PVs have been found in cats, suggesting cross-species transmission (Anis et al., 2010; O’Neill et al., 2011). However, the detection of human PVs might be due to cross-contamination during sampling or processing of samples (Munday and Thomson, 2021). PV infection has also been detected in other felids, including the Florida panther subspecies of cougar (Puma concolor coryi), Bobcat (Lynx rufus), Asian lion (Panthera leo persica), Snow leopard (Panthera unica), clouded leopard (Neofelis nebulosa), and cheetah (Sundberg et al., 2000; Wolfe and Spraker, 2007; Mitsouras et al., 2011; Orbell et al., 2011; Steenkamp et al. 2022).

Pathogenesis

Papillomaviruses are epitheliotropic; infections usually occur through lesions or abrasions of the skin. Initially, the basal cells of the stratum germinativum (stratum basale, Fig. 2) are infected, which leads to hyperplasia and delayed maturation of cells in the stratum spinosum and stratum granulosum. In the basal cells only early gene expression occurs, and these cells allow persistence of PV infection. Viral protein (L1 and L2) synthesis and virion assembly occur in terminally differentiated cells of the stratum spinosum and, more specifically, the stratum granulosum. Virus is present in the differentiated keratinized cells and is shed with exfoliated cells of the stratum corneum.

                      Fig. 2. Different layers of the skin

Due to their ability to alter cell regulation, PVs can also induce tumours. PV is one of the most common causes of viral neoplasia in humans and has also been associated with neoplasia in dogs, horses, ruminants, and pigs. Both E6 and E7 are considered oncogenes, expressing proteins that inhibit the retinoblastoma (pRB) and p53 protein, respectively, resulting in interference with normal cell regulation leading to malignant lesions (Altamura et al., 2016). PV are, however, commonly found in the normal skin of different animals, including the cat (Munday and Witham, 2010); this makes definitive proof of a causal relationship between the presence of PV sequences and skin lesions difficult.

Immunity

Papillomaviruses tend to stimulate a mild immune response due to viral replication in the superficial layers of the epithelium. If an effective immune response is induced, it is based on cell-mediated immunity (Jain et al., 2006; Munday and Thomson, 2021). This leads to the lysis of infected cells and resolution of the hyperplastic lesions. Antibodies can be induced but seem not to play a role in lesion resolution. However, antibodies can play a role in the type-specific protection against (re)infection (Ghim et al., 2000).

Clinical signs

The majority of cats are infected by PVs, but disease seems to occur less frequently compared to other domestic animals (Munday, 2014; Munday and Thomson, 2021). Nevertheless, several diseases have been associated with different types of PVs. Lesions reported to be associated with PVs in domestic cats include hyperplastic plaques, skin papillomas, oral papillomas, Bowenoid in situ carcinomas (BISCs), cutaneous and oral squamous cell carcinomas ((O)SCCs), feline basal cell carcinomas, and feline sarcoids. Also, there is evidence for the involvement of FcaPV2 in the development of MCC in cats (Ito et al., 2022).

Hyperkeratotic plaques

Cutaneous hyperkeratotic plaques seem to be most common in older and immunosuppressed cats, e.g. FIV-infected animals (Carney et al., 1990; Egberink et al., 1992). However, plaques have also been reported in cats without any recognized immunodeficiency (Wilhelm et al., 2006). The plaques appear as flat, slightly raised, scaly and variably pigmented lesions and are generally less than 1 cm in diameter (Fig. 3).

Fig. 3. Pigmented flat cutaneous papillomas (photo Herman Egberink, Ph.D. thesis Utrecht)

Feline catus PVs 2, 3 and 5 have been associated with viral plaques (Munday et al., 2017b; Munday and Peters-Kennedy, 2010). The lesions share many histological features with BISCs, and are thought to be precursors of BISC, representing different severities of the same disease (Wilhelm et al., 2006).

Skin papillomas (warts)

Papillomas of the skin, characterized by marked thickening and folding of the epidermis, seem to be rare in cats, in contrast to dogs and other domestic animals. To date only three cases of PV-induced cutaneous papillomas have been reported in domestic cats. In one cat with a focal area of hyperplasia on the eyelid, PV L1 was detected in the skin lesion by immunostaining (Carpenter et al., 1992). In a cat with a papilloma that developed on the nasal planum only, sequences from human PV type 9 could be amplified (Munday et al., 2007). PVs are usually highly species-specific, and detection of these human PV type sequences might be due to cross-contamination and not cross-infection. Humans are ubiquitously and asymptomatically infected, which can lead to sample contamination. The third case was a 4.5-year-old, male domestic shorthair cat with a papilloma on the nasal planum. The PV DNA sequence amplified from the lesion had a low similarity to other feline PV types, suggestive of a novel PV genus (Munday et al., 2022b).

Oral papillomas

Only a few cases of oral papillomas have been described in cats; they seem to occur less frequently than in other species (Munday et al., 2015). However, because those papillomas seem to be restricted to the ventral surface of the tongue, it was suggested that they might occur more frequently but remain undetected (Munday and Thomson, 2021). The lesions appear as clusters of exophytic lesions and are found on the ventral surface of the tongue. They are characterized histologically by foci of markedly hyperplastic folded epithelium with PV-induced cell changes. In a report describing two cats, oral papillomas were associated with FcaPV1 (Munday et al., 2015). This feline PV type is the only feline type classified within the genus lambdapapillomavirus to which the PV types that cause oral papillomas in dogs and some other species also belong (Munday and Thomson, 2021).

Bowenoid in situ carcinomas (BISCs)

Feline BISCs are superficial lesions that are confined to the epidermis and occur often in pigmented, haired skin as crusting, de- or hyperpigmented and roughly circular lesions (Wilhelm et al., 2006). BISCs tend to be larger then viral plaques, and are more markedly raised (Munday and Wilhelm, 2020). The lesions are typically found in middle-aged or older cats (Wilhelm et al., 2006). Spontaneous regression can occur, although many BISCs persist and some progress to an invasive squamous cell carcinoma (ISCC). Devon Rex and Sphynx breeds seem to be more prone to developing BISC: lesions develop at an earlier age and also tend to be more aggressive, rapidly progressing to ISCC and metastatic SCC (Ravens et al., 2013; Munday et al., 2016).

A clear association between PV DNA (the then-called Felis domesticus papillomavirus 2; FdPV-2) and feline SCCs has been found; DNA was detected in all 20 BISCs examined, and in 17 out of 20 cases of SCCs (Munday et al., 2008). However, FdPV-2 DNA was also detected in 52% of normal skin swabs (Munday and Witham, 2010). Although FdPV-2 has been detected most frequently in BISCs and SCCs, other PV types and FcaPV3, FcaPV4 and FcaPV5 were identified as well (Munday et al., 2013a; Munday et al., 2018; Vascellari et al., 2019).

Feline cutaneous squamous cell carcinomas (SCCs)

Cutaneous SCCs are common skin cancers in cats. Sunlight plays a role in their development. Lesions tend to be found in sparsely haired areas such as the eyelids, nose, and pinnae and typically occur in non-pigmented skin. A contributory role for FcaPV is suggested by the more frequent detection of FcaPV2 DNA in cutaneous SCCs than in the normal skin of cats (Munday et al., 2008; Munday et al., 2011b). The relative roles of ultraviolet (UV) light, other co-factors, or FcaPV infection in the development of SCCs is uncertain (Munday and Thomson, 2021). Studies suggest that FcaPVs could have an aetiological role in a quarter to a third of all cutaneous SCCs (Munday et al., 2011b; Hoggard et al., 2018; Munday et al., 2019). Besides the more frequent detection of FcaPV2 in SCC lesions, other studies support its role in the development of SCCs. Firstly, higher viral loads have been detected in BISCs and in a subset of SCCs than in normal skin (Thomson et al., 2016). Secondly, FcaPV2 RNA, as evidence of gene expression, has been detected in a proportion of SCCs but not in normal skin (Altamura et al., 2016; Thomson et al., 2016). Also, staining for p16^CDKN2A protein can be visualized in SCCs that also contain PV DNA (see “diagnosis” section later) (Munday et al., 2011a; Munday et al., 2013b). Feline PV type 2 is the most common type of PV detected in cutaneous SCCs but, in some cases of SCCs, FcaPV3, FcaPV4 or FcaPV6 DNA have been identified (Yamashita-Kawanishi et al., 2018; Vascellari et al., 2019; Yamashita-Kawanishi et al., 2021b). In one study 50% of the sequenced PV DNA was most closely related to human PV DNA (O’Neill et al., 2011).

Oral squamous cell carcinomas (OSCCs)

Feline oral SCCs are aggressive invasive neoplasms and an important cause of mortality (Munday et al., 2019; Munday and Thomson, 2021). They appear as multiple exophytic filiform masses on the central surface of the tongue (Munday et al., 2019). In humans, PV is an established cause of a proportion of the OSCCs. Consequently, several studies on the aetiology of feline OSCCs have focused on the detection of PV in OSCC lesions. Results of these studies show significant differences in the detection of PV DNA within feline OSCCs, as described below.

Papillomavirus DNA could not be detected in any of 30 cases of OSCC from cats in New Zealand nor in seven OSCCs samples screened in cats from Japan (Munday et al., 2011c; Yamashita-Kawanishi et al., 2018). In cats in New Zealand, FcaPV1 DNA was found in only one of 36 samples, and also in one of 16 samples from cats with feline chronic gingivostomatitis (FCGS) (Munday and French, 2015). Using a metagenomic approach for DNA viruses, the virome was sequenced and FcaPV3 was detected in only one of 20 OSCC samples and none of 9 samples of normal gingiva (Chu et al., 2020). These findings are in contrast to the results of other studies. In a study performed in Italian cats, a higher number of samples from cats with OSCC and FCGS were positive for FcaPV2 DNA, namely 10 of 32 (31%) and 4 of 11 (36%), respectively (Altamura et al., 2020). The presence of viral gene expression suggested active viral replication, but no significant differences in viral loads were detected between the samples of OSCC and FCGS. In a recent study, 11 of 19 (57.9%) OSCC samples of cats from Taiwan and one of 9 (11.1%) OSCC sample of cats from Japan contained FcaPV2 DNA, but no oral samples from cats without OSCC samples were included (Yamashita-Kawanishi et al., 2021a). In conclusion, the markedly different results of detection of numbers of PV-positive OSCC samples along with similar detection rates in non-neoplastic samples seem, so far, not to support a role for PV in the development of OSCCs.

Feline Basal Cell Carcinomas (BCC)

Basal cell carcinomas are rare feline skin neoplasms presenting mostly as single ulcerated raised plaques or nodules; keratinization is generally absent (Munday et al., 2019). An association between PV infection and feline BCC was suggested by the presence of PV cytopathic changes in cells within BCCs (Munday and Thomson, 2021). The association was further supported by the detection of FcaPV3 DNA in a cat with multiple BCCs (Munday et al., 2018) and the amplification of sequences from a feline BCC of a probably novel type of PV that was not further classified (Munday et al., 2017c). A novel type was amplified from a BCC and was designated FcaPV7 and considered to be associated with the skin cancer. The histological lesions were different from those reported with other subtypes of FcaPV (Munday et al., 2023).

Feline cutaneous fibropapillomas or feline sarcoids

Feline sarcoids are rare, presenting as skin neoplasms; solitary or multiple non-ulcerated nodular masses are found most commonly on the head (nasal philtrum, lips), neck, ventral abdomen and limbs (Fig. 4).

Fig. 4. A case of sarcoid in a patient presented at the Utrecht Companion Animal Clinic; diagnosis was verified histologically, but the viral etiology was not established (courtesy Y.Schlotter, Companion Animal Clinic, Veterinary Faculty, Utrecht University)

Lesions are characterized by proliferation of mesenchymal rather than epithelial cells. Metastasis does not occur (Luff and Munday, 2023).The finding of a PV similar to BPV type 14 (BPV14) and the higher prevalence in cats with known exposure to cattle suggests an association with the bovine virus (Schulman et al., 2001; Munday et al., 2010). Also, PV DNA could be localized in neoplastic mesenchymal cells by in situ hybridization (ISH) (Teifke et al., 2003). This hypothesis is in line with the known association between BPV and equine sarcoids (Ogłuszka et al., 2021).

Merkel cell carcinoma (MCC)

Merkel cell carcinoma is a rare and aggressive neuroendocrine carcinoma of the skin. In humans, Merkel cell polyomavirus (MCPyV) is involved in approximately 80% of Merkel cell carcinomas, and in 20% of cases UV light exposure plays a role (Dellambra et al., 2021). Tumourigenesis is caused by the integration of the MCPyV DNA into the host genome and induction of persistent expression of viral oncogenes or through the occurrence of DNA mutations induced by UV exposure (Feng et al., 2008; Dellambra et al., 2021). Feline MCCs are rare skin tumours, located in the dermis and/or subcutis and present as firm, red, dome-shaped, solitary skin nodules. The overlying skin is frequently ulcerated (Sumi et al., 2018). The tumours are characterized by the expression of some epithelial markers (cytokeratin 18 and 20) and neuroendocrine markers, such as synaptophosyn and CD56 (Sumi et al., 2018). Cats with MCC often have other proliferative skin lesions such as SCC and BCC, and a role for FcaPV2 in feline MCC has also been suggested (Ito et al., 2022). FcaPV DNA could be detected in 95% of feline MCC cases and the presence of FcaPV DNA in the tumour cells was confirmed by ISH (Ito et al., 2022). The hybridization signal pattern suggested the integration of the DNA into the genome, which was further evidenced by whole genome sequencing of two FcaPV-positive cases (Ito et al., 2023).

Table 1. Papillomavirus lesions and their associated papillomavirus type

FcaPV indicates Feline catus papillomavirus
HuPV indicates human papillomavirus
BPV indicates bovine papillomavirus

Table 2. Papillomavirus lesion and clinical presentation

ISCC: invasive squamous cell carcinoma

Diagnosis

Several methods can support a diagnosis of a viral-induced hyperplastic lesion. A biopsy from a skin lesion can be taken for histopathologic examination and immunohistochemical staining of PV group-specific antigens (Munday and Thomson, 2021). The different PV-induced lesions of virally-induced oral papillomas, BISCs, and feline sarcoids all show characteristic histological changes, often related to the PV-type involved (Munday and Thomson, 2021). Infection of cells with FcaPV1 can result in eosinophilic intracytoplasmic bodies (Munday et al., 2015), infection with FcaPV2, in expanded cytoplasm by clear or slightly granular grey-blue material, and with FcaPV3, slender elongated perinuclear basophilic bodies (Munday et al., 2022a). In cells infected with FcaPV4 or FcaPV5 the cytoplasm may be expanded by dark blue-grey material (Dunowska et al., 2014; Munday et al., 2017a). These changes become less visible in advanced neoplastic lesions where there is less, or no, viral replication. In lesions with PV-induced cell changes, antibodies against the L1 protein can be used to stain the PV protein within cells. However, feline PV-type specific antibodies are not commercially available and antibodies against PV types of other species (including humans) might not cross-react; if the cross-reactivity with feline type PVs is unknown, a negative result will be difficult to interpretate (Munday and Thomson, 2021). Immunostaining is of no use in PV-induced cancers since viral replication in these lesions is rare. However, in these lesions, immunostaining of p16^CDKN2A protein (p16) can be performed as a proxy marker for PV-induced SCCs (Cunningham Jr et al., 2006). The p16 inhibits the retinoblastoma protein (pRB) to prevent cell division. In PV-induced neoplasms, the pRB is degraded, which leads to the loss of pRB and increased amounts of p16 (Munday and Thomson, 2021). A strong association between the presence of PV-DNA and p16 immunostaining has been shown (Munday et al., 2011b; Thomson et al., 2016). Also, PCR can be used to demonstrate PV DNA in the lesions and to identify the viral strain by further sequencing. However, the presence of PV DNA in the normal skin of cats makes interpretation of positive PCR results of skin lesions difficult. Therefore, a positive PCR is not definitive proof that the lesion is caused by PV if DNA is extracted from the whole sample. In contrast to PCR, ISH detects PV DNA or RNA within the cells of a lesion, and presence of PV DNA or RNA in the basal and suprabasilar epithelial layers of the lesion supports a role of the virus in the pathogenesis (Munday and Thomson, 2021).

Treatment

No specific treatment for feline PV-induced skin lesions is known. In immunocompetent cats, spontaneous regression can be expected, similar to dogs, but it might take up to several months. The treatment of superficial layers of the skin can be sufficient for lesions that are confined to the epidermis, like BISCs. Imiquimod cream stimulates inflammation and is used for the topical treatment of Bowen’s disease in humans. The cream has never been thoroughly evaluated in cats with this condition; a response was noted but no conclusion with respect to the efficacy of the drug in cats has been reached (Gill et al., 2008). In this study, the SSC lesions were also PV antigen-negative. Although anecdotal evidence supports the use of this medication, more controlled studies are required to evaluate the safety and efficacy of this treatment. If only a few superficial lesions are present, surgical excision can be considered assuming that all of the affected epidermis can be removed (Munday and Thomson, 2021). Carbon dioxide laser therapy, which has been used in other species, can also be considered (Knight et al., 2016), particularly in areas where wound closure is difficult. Cryotherapy can also be used to treat the superficial lesions (Munday and Thomson, 2021). Feline ISCCs tend to slowly metastasize. Therefore, if anatomical location allows, complete excision might be curative.

Prognosis

Most PV infections remain asymptomatic with limited replication in epithelial cells. Cutaneous and oral papillomas often resolve spontaneously. The prognosis of PV-induced SCCs depends on the number, location and invasiveness of the lesions. PV-induced SCCs tend to have a more favourable prognosis than non-PV-associated SCCs (Luff and Munday, 2023). If successfully treated e.g. by excision of the lesion, new additional lesions might develop in the same cat. Sphinx and Devon Rex cats are predisposed to BISCs and have a higher risk of developing invasive and metastatic SCCs (Munday et al., 2016). Therefore, all viral plaques/BISCs should be carefully monitored for progression to SCC. Feline OSCCs are almost invariably fatal, but no association of feline OSCCs with PV infection has been proven.

Vaccination

Although vaccination against PV infections can be effective, as evidenced by the use of successful vaccines in humans, no vaccines are available for papillomatosis in cats. In one study, an experimental FcaPV2 virus-like particle vaccine was shown to be safe and immunogenic (Thomson et al., 2019), but vaccination-induced high antibody titres had no effect on the viral loads in cats that were already infected (Thomson et al., 2019). The majority of PV-induced lesions in cats are caused by FcaPV2, which infects cats within the first few days of life (Thomson et al., 2015). To prevent disease development, a FcaPV2 vaccination would need to be given before infection, which is not feasible due to early infection. Vaccines against other PV types are unlikely to be developed because of the development costs together with the relatively rare occurrence of PV-induced disease by these virus types (Munday and Thomson, 2021).

Acknowledgement

ABCD Europe gratefully acknowledges the support of Boehringer Ingelheim (the founding sponsor of the ABCD), Virbac and MSD Animal Health.

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Munday JS, Dunowska M, Hills SF, Laurie RE (2013a): Genomic characterization of Felis catus papillomavirus-3: A novel papillomavirus detected in a feline Bowenoid in situ carcinoma. Veterinary Microbiology 165, 319-325. doi:10.1016/j.vetmic.2013.04.006.

Munday JS, Fairley RA, Mills H, Kiupel M, Vaatstra BL (2015): Oral Papillomas Associated With Felis catus Papillomavirus Type 1 in 2 Domestic Cats. Veterinary Pathology 52, 1187-1190. doi:10.1177/0300985814565133.

Munday JS, French AF (2015): Felis catus papillomavirus types 1 and 4 are rarely present in neoplastic and inflammatory oral lesions of cats. Research in Veterinary Science 100, 220-222. doi:10.1016/j.rvsc.2015.03.002.

Munday JS, French AF, Gibson IR, Knight CG (2013b): The Presence of p16CDKN2A Protein Immunostaining Within Feline Nasal Planum Squamous Cell Carcinomas Is Associated With an Increased Survival Time and the Presence of Papillomaviral DNA. Veterinary Pathology 50, 269-273. doi:10.1177/0300985812452582.

Munday JS, French AF, Peters-Kennedy J, Orbell GM, Gwynne K (2011a): Increased p16CDKN2A protein within feline cutaneous viral plaques, bowenoid in situ carcinomas, and a subset of invasive squamous cell carcinomas. Veterinary Pathology 48, 460-465. doi:10.1177/0300985810374844.

Munday JS, French A, Thomson N (2017c): Detection of DNA sequences from a novel papillomavirus in a feline basal cell carcinoma. Veterinary Dermatology 28, 236-e260. doi:10.1111/vde.12402.

Munday JS, Gedye K, Knox MA, Pfeffer H, Lin X (2023): Genetic characterisation of Felis catus papillomavirus type 7, a rare infection of cats that may be associated with skin cancer. Vet Microbiol 284, 109813. doi:10.1016/j.vetmic.2023.109813.

Munday JS, Gibson I, French AF (2011b): Papillomaviral DNA and increased p16CDKN2A protein are frequently present within feline cutaneous squamous cell carcinomas in ultraviolet-protected skin. Veterinary Dermatology 22, 360-366. doi:10.1111/j.1365-3164.2011.00958.x.

Munday JS, Hanlon EM, Howe L, Squires RA, French AF (2007): Feline cutaneous viral papilloma associated with human papillomavirus type 9. Veterinary Pathology 44, 924-927. doi:10.1354/vp.44-6-924.

Munday JS, Hunt H, Orbell G, Pfeffer H (2022a): Detection of a Novel Papillomavirus Type within a Feline Cutaneous Basal Cell Carcinoma. Veterinary Sciences 9 (art. 671). doi:10.3390/vetsci9120671.

Munday JS, Kiupel M (2010): Papillomavirus-associated cutaneous neoplasia in mammals. Veterinary Pathology 47, 254-264. doi:10.1177/0300985809358604.

Munday JS, Kiupel M, French AF, Howe L (2008): Amplification of papillomaviral DNA sequences from a high proportion of feline cutaneous in situ and invasive squamous cell carcinomas using a nested polymerase chain reaction. Veterinary Dermatology 19, 259-263.

Munday JS, Knight CG, French AF (2011c): Evaluation of feline oral squamous cell carcinomas for p16CDKN2A protein immunoreactivity and the presence of papillomaviral DNA. Research in Veterinary Science 90, 280-283. doi:10.1016/j.rvsc.2010.06.014.

Munday JS, Knight CG, Howe L (2010): The same papillomavirus is present in feline sarcoids from North America and New Zealand but not in any non-sarcoid feline samples. Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc 22, 97-100.

Munday J, Marshall S, Thomson N, Kiupel M, Heathcott R, French A (2017a): Multiple viral plaques with sebaceous differentiation associated with an unclassified papillomavirus type in a cat. New Zealand Veterinary Journal:1-5. doi:10.1080/00480169.2017.1313146.

Munday JS, Peters-Kennedy J (2010): Consistent detection of Felis domesticus papillomavirus 2 DNA sequences within feline viral plaques. Journal of Veterinary Diagnostic Investigation 22, 946-948. doi: 10.1177/104063871002200615

Munday JS, Sharp CR, Beatty JA (2019): Novel viruses: Update on the significance of papillomavirus infections in cats. Journal of Feline Medicine and Surgery 21, 409-418. doi:10.1177/1098612X18808105.

Munday JS, Thomson NA (2021): Papillomaviruses in Domestic Cats. Viruses 13, 1664. doi:10.3390/v13081664.

Munday JS, Thomson NA, Henderson G, Fairley R, Orbell GM (2018): Identification of Felis catus papillomavirus 3 in skin neoplasms from four cats. Journal of Veterinary Diagnostic Investigation 30, 324-328. doi:10.1177/1040638717750852.

Munday JS, Thomson NA, Luff JA (2017d): Papillomaviruses in dogs and cats. Veterinary Journal 225, 23-31. doi:10.1016/j.tvjl.2017.04.018.

Munday JS, Wilhelm S (2020): Viral Diseases. Pages 359-385 in Noli C, Colombo S, eds. Feline Dermatology. Cham: Springer International Publishing.

Munday JS, Witham AI (2010): Frequent detection of papillomavirus DNA in clinically normal skin of cats infected and noninfected with feline immunodeficiency virus. Veterinary Dermatology 21, 307-310. doi:10.1111/j.1365-3164.2009.00811.x.

Munday JS, Wong AK, Julian AF (2022b): Cutaneous papilloma associated with a novel papillomavirus sequence in a cat. Journal of Veterinary Diagnostic Investigation 34, 902-904. doi:10.1177/10406387221107152.

O’Neill SH, Newkirk KM, Anis EA, Brahmbhatt R, Frank LA, Kania SA (2011): Detection of human papillomavirus DNA in feline premalignant and invasive squamous cell carcinoma. Veterinary Dermatology 22, 68-74. doi:10.1111/j.1365-3164.2010.00912.x.

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Orbell GMB, Young S, Munday JS (2011): Cutaneous sarcoids in captive African lions associated with feline sarcoid-associated papillomavirus infection. Veterinary Pathology 48, 1176-1179. doi.org/10.1177/0300985810391111.

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Thomson NA, Dunowska M, Munday JS (2015): The use of quantitative PCR to detect Felis catus papillomavirus type 2 DNA from a high proportion of queens and their kittens. Veterinary Microbiology 175, 211-217. doi:10.1016/j.vetmic.2014.11.028.

Thomson NA, Howe L, Weidgraaf K, Thomas DG, Young V, Ward VK, Munday JS (2019): Felis catus papillomavirus type 2 virus-like particle vaccine is safe and immunogenic but does not reduce FcaPV-2 viral loads in adult cats. Veterinary Immunology and Immunopathology 213, 109888. doi:10.1016/j.vetimm.2019.109888.

Thomson NA, Munday JS, Dittmer KE (2016): Frequent detection of transcriptionally active felis catus papillomavirus 2 in feline cutaneous squamous cell carcinomas. Journal of General Virology 97, 1189-1197. doi:10.1099/jgv.0.000416.

Vascellari M, Mazzei M, Zanardello C, Melchiotti E, Albanese F, Forzan M, Croce MF, Alberti A, Abramo F (2019): Felis catus Papillomavirus Types 1, 2, 3, 4, and 5 in Feline Bowenoid in Situ Carcinoma: An In Situ Hybridization Study. Veterinary Pathology 56, 818-825. doi:10.1177/0300985819859874.

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Yamashita-Kawanishi N, Chang CY, Chambers JK, Uchida K, Sugiura K, Kukimoto I, Chang HW, Haga T (2021a): Comparison of prevalence of felis catus papillomavirus type 2 in squamous cell carcinomas in cats between Taiwan and Japan. Journal of Veterinary Medical Science 83, 1229-1233. doi:10.1292/jvms.21-0153.

Yamashita-Kawanishi N, Gushino Y, Chang CY, Chang HW, Chambers JK, Uchida K, Haga T (2021b): Full-genome characterization of a novel Felis catus papillomavirus 4 subtype identified in a cutaneous squamous cell carcinoma of a domestic cat. Virus Genes 57, 380-384. doi:10.1007/s11262-021-01843-y.

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