Background. Correlating human papillomavirus (HPV) type with the clinical and histopathological features of skin lesions (from genital and nongenital sites) can present a diagnostic challenge. Objective. In this study, HPV infection patterns were correlated with pathology and clinical presentation in lesional and nonlesional body sites from a young patient with a primary T-cell immunodeficiency. Methods. HPV infection was evaluated at both DNA and protein levels by polymerase chain reaction and immunohistochemistry. Results. The patient’s genital lesions were caused exclusively by α-genotypes (high-risk type HPV-51 in the anal and low-risk type HPV-72 in the penile condylomas). The opposite was true for the skin lesions, which were infected by β-genotypes alone (HPV-8 and HPV-24). HPV-24 was the predominant type in terms of viral load, and the only one found in productive areas of infection. The patient had already developed high-grade dysplasia in the anal condyloma-like lesions, and showed areas of early-stage dysplasia in the lesions caused by the β-genotype HPV-24. Limitations. The basic origin of the immunodeficiency is not yet defined. Conclusion. These findings provide proof of principle that both α- and β-genotypes can cause overt dysplastic lesions when immunosurveillance is lost, which is not restricted to epidermodysplasia verruciformis.

α- and β-Papillomavirus infection in a young patient with an unclassified primary T-cell immunodeficiency and multiple mucosal and cutaneous lesions

LANDINI, Manuela Miriam;DE ANDREA, Marco;
2014

Abstract

Background. Correlating human papillomavirus (HPV) type with the clinical and histopathological features of skin lesions (from genital and nongenital sites) can present a diagnostic challenge. Objective. In this study, HPV infection patterns were correlated with pathology and clinical presentation in lesional and nonlesional body sites from a young patient with a primary T-cell immunodeficiency. Methods. HPV infection was evaluated at both DNA and protein levels by polymerase chain reaction and immunohistochemistry. Results. The patient’s genital lesions were caused exclusively by α-genotypes (high-risk type HPV-51 in the anal and low-risk type HPV-72 in the penile condylomas). The opposite was true for the skin lesions, which were infected by β-genotypes alone (HPV-8 and HPV-24). HPV-24 was the predominant type in terms of viral load, and the only one found in productive areas of infection. The patient had already developed high-grade dysplasia in the anal condyloma-like lesions, and showed areas of early-stage dysplasia in the lesions caused by the β-genotype HPV-24. Limitations. The basic origin of the immunodeficiency is not yet defined. Conclusion. These findings provide proof of principle that both α- and β-genotypes can cause overt dysplastic lesions when immunosurveillance is lost, which is not restricted to epidermodysplasia verruciformis.
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http://www.sciencedirect.com/science/article/pii/S0190962214009426
Papillomavirus; Skin cancer; viral carcinogenesis; primary immunodeficiency; viral life cycle
Manuela M. Landini;Cinzia Borgogna;Alberto Peretti;Enrico Colombo;Elisa Zavattaro;Renzo Boldorini;Umberto Miglio;John Doorbar;Paolo Ravanini;Rajesh Kumar;Daniele Moratto;Raffaele Badolato;Marco De Andrea;Marisa Gariglio
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2318/146636
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