Characterization of Two HPV-3 Related Papillomaviruses from Common Warts That Are Distinct Clinically from Flat Warts or Epidermodysplasia Verruciformis
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Epidermodysplasia verruciformis
Bovine papillomavirus
Common warts
Sequence homology
Homology
Papillomaviridae
Genital warts
Cleavage (geology)
Human papillomavirus (HPV) is a DNA tumor virus strongly associated with cervical neoplasias. There are over 80 different types of HPVs which can infect either mucosal or cutaneous tissue. Cutaneous squamous cell carcinomas (SCC) associated with HPV are often seen in patients with epidermodysplasia verruciformis (EV). EV is characterized by cutaneous lesions that progress to SCC upon UV exposure. In characterizing the HPV types associated with an unusually aggressive form of EV, we have cloned an HPV with homology to the moderately oncogenic genital type HPV 34, the oncogenic EV type HPV 5 and from benign oral mucosal type HPV 32. The presence of sequences from these highly divergent types is a novel finding. These three viral types are from different phylogenetic branches of the HPV family believed to have evolved independently from each other.
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Epidermodysplasia verruciformis
Common warts
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To the Editor.—
The immune system plays an important role in the control of common viral wart infections. Both serum antibody as well as cell-mediated factors participate in the host's response to the wart virus.1Extensive persistent verrucae have been associated with immunodeficiency.2,3Therapy of the aggressive recalcitrant wart infections in immunosuppressed patients is often difficult. Recently, however, good results have been reported in patients with epidermodysplasia verruciformis, sarcoidosis, and leukemia using etretinate.4-7We describe herein an immunodeficient patient with a large disabling wart on the foot, previously refractory to treatment, who responded to isotretinoin therapy.Report of a Case.—
In 1975, a 27-year-old man was diagnosed as having Hodgkin's disease and was successfully treated with chemotherapy. Since completion of the initial chemotherapy, he had no evidence of recurrence of disease. About one year following the completion of the chemotherapy he began to develop common warts onEpidermodysplasia verruciformis
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Epidermodysplasia verruciformis
Bovine papillomavirus
Common warts
Sequence homology
Homology
Papillomaviridae
Genital warts
Cleavage (geology)
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Epidermodysplasia verruciformis (EV) is a rare human genetic predisposition to develop flat warts, some of which subsequently undergo cancer transformation. Some human papillomaviruses (HPVs), i.e. HPV 5 and 8, have been associated with cancer development as a sequela of EV. As similar diseases have been observed in dogs, it was hypothesized that unknown canine papillomaviruses (CPVs) may exist and that they may be present in cases of canine EV. Consequently, DNA was extracted from a malignant lesion of a dog with EV and circular DNA was amplified by multiple-primed rolling-circle amplification (RCA). Indeed, sequence determination and analysis of the RCA-amplified and cloned DNA from a malignant canine EV lesion resulted in the detection and primary description of a third CPV (CPV3). Typical papillomavirus genes were identified, with deduced amino acid similarities ranging from 20 to 57 % for E1, E2, E6, E7, L1 and L2, respectively. According to the sequence of the L1 gene, which is used for papillomavirus classification, the new isolate meets the majority of criteria needed to declare detection of a novel genus among the papillomaviruses. Thus, CPV3 may represent the prototype of this novel genus. As the novel virus was found in a dog in association with lesions reminiscent of human EV, it should be interesting to test in the future whether this condition can be reproduced in experimental animals. If such were the case, a new model for EV could be established.
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ABSTRACT The role of human papillomavirus (HPV) in anogenital carcinogenesis is firmly established, but evidence that supports a similar role in skin remains speculative. Immunosuppressed renal transplant recipients have an increased incidence of viral warts and nonmelanoma skin cancer, and the presence of HPV DNA in these lesions, especially types associated with the condition epidermodysplasia verruciformis (EV), has led to suggestions that HPV may play a pathogenic role. However, differences in the specificities and sensitivities of techniques used to detect HPV in skin have led to wide discrepancies in the spectrum of HPV types reported. We describe a degenerate nested PCR technique with the capacity to detect a broad spectrum of cutaneous, mucosal, and EV HPV types. In a series of 51 warts from 23 renal transplant recipients, this method detected HPV DNA in all lesions, representing a significant improvement over many previously published studies. Cutaneous types were found in 84.3% of warts and EV types were found in 80.4% of warts, whereas mucosal types were detected in 27.4% of warts. In addition, the method allowed codetection of two or more distinct HPV types in 94.1% of lesions. In contrast, single HPV types were detected in all but 1 of 20 warts from 15 immunocompetent individuals. In summary, we have established a highly sensitive and comprehensive degenerate PCR methodology for detection and genotyping of HPV from the skin and have demonstrated a diverse spectrum of multiple HPV types in cutaneous warts from transplant recipients. Studies designed to assess the significance of these findings to cutaneous carcinogenesis are under way.
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We describe a 67-year-old woman with disseminated warts which she had had for more than 38 years. The lesions consisted of common and plane warts, wart-like plaques and red-brownish macules similar to those in pityriasis versicolor. Furthermore, during follow-up, several solar keratoses, plaques of Bowen's disease and invasive squamous cell carcinomas were excised. The patient also had T-cell immunodeficiency of unknown aetiology. Histopathology demonstrated that all the warts showed the cytopathological features of common warts, but not those of the warts in epidermodysplasia verruciformis (EV). We investigated the presence of human papillomavirus (HPV) DNA in the warts by blot hybridization and molecular cloning and found that the lesions harboured HPV 2, but not EV–HPVs or other HPVs. In addition, the histopathological distribution of the viral DNA was confirmed in paraffin sections of warts from the patient at different ages by in situ hybridization. However, these investigations yielded negative results in specimens of Bowen's disease and invasive squamous cell carcinoma. These results demonstrated that the patient had been infected with HPV 2 from childhood, but the negative results for detection of DNA of HPV 2 in carcinomas from the patient do not support an oncogenic potential for HPV 2. In conclusion, HPV 2, an aetiological agent of common warts in the general population, may induce a lifelong severe verrucosis in some immunosuppressed patients.
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Common warts
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Histopathology
Papillomaviridae
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Epidermodysplasia verruciformis
Common warts
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The late gene promoter P7535 of the epidermodysplasia verruciformis-associated human papillomavirus type 8 (HPV8) is regulated by the viral E2 protein. Transfection experiments performed with the human skin keratinocyte cell line RTS3b and P7535 reporter plasmids revealed transactivation at low amounts and a repression of basal promoter activity at high amounts of E2 expression vector. This repression was promoter specific and correlated with the amount of transiently expressed E2 protein. Mutational analyses revealed that the negative regulation of P7535 activity is mediated by the low-affinity E2 binding site P2, which is separated by one nucleotide from the P7535 TATA box. Biochemical and genetic analyses suggested that repression is due to a displacement of the TATA-box binding protein by E2 and an interference of E2 with promoter-activating cellular factors that specifically recognize the P2 sequence. The high conservation of the P2 sequence among several papillomaviruses (epidermodysplasia verruciformis-associated HPVs, HPV1, cottontail rabbit papillomavirus, and bovine papillomavirus type 1) in the vicinity of the late gene promoter cap site suggests that an interplay of E2 and cellular factors at this sequence element is important for the expression of structural proteins.
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Bovine papillomavirus
TATA box
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