Lucia Oton-Gonzalez1, John Charles Rotondo1, Luca Cerritelli2, Nicola Malagutti2, Carmen Lanzillotti1, Ilaria Bononi1, Andrea Ciorba2, Chiara Bianchini2, Chiara Mazziotta1, Monica De Mattei1, Stefano Pelucchi2, Mauro Tognon3, Fernanda Martini4. 1. Department of Medical Sciences, Laboratories of Cell Biology and Molecular Genetics, School of Medicine, University of Ferrara, 64/B, Fossato di Mortara Street, 44121, Ferrara, Italy. 2. Department of Biomedical Sciences and Specialistic Surgeries, ENT Section, University of Ferrara and University Hospital of Ferrara, 8, Aldo Moro Square, 44124, Cona, Italy. 3. Department of Medical Sciences, Laboratories of Cell Biology and Molecular Genetics, School of Medicine, University of Ferrara, 64/B, Fossato di Mortara Street, 44121, Ferrara, Italy. tgm@unife.it. 4. Department of Medical Sciences, Laboratories of Cell Biology and Molecular Genetics, School of Medicine, University of Ferrara, 64/B, Fossato di Mortara Street, 44121, Ferrara, Italy. mrf@unife.it.
Abstract
BACKGROUND: Killian polyp (KP) is a benign lesion that arises from the maxillary sinus. The etiology of KP is unknown. The aim of this study was to investigate the potential involvement of human papilloma- (HPV) and polyoma-viruses (HPyV) infections in the onset of KP. METHODS: DNA from antral (n = 14) and nasal (n = 14) KP fractions were analyzed for HPV and HPyV sequences, genotypes, viral DNA load and physical status along with expression of viral proteins and p16 cellular protein. RESULTS: The oncogenic HPV16 was detected in 3/14 (21.4%) antral KPs, whilst nasal KPs tested HPV-negative (0/14). The mean HPV16 DNA load was 4.65 ± 2.64 copy/104 cell. The whole HPV16 episomal genome was detected in one KP sample, whereas HPV16 DNA integration in two KPs. P16 mRNA level was lower in the KP sample carrying HPV16 episome than in KPs carrying integrated HPV16 and HPV- negative KPs (p< 0.001). None of the antral and nasal KP samples tested positive for HPyV DNA (0/28). CONCLUSIONS: A fraction of KP tested positive for the oncogenic HPV16. HPV16 detection in the KP antral portion may be consistent with HPV16 infection derived from the maxillary sinus. HPV16 DNA integration represents a novel finding. Altogether, these data improve our knowledge on the association between KP and HPV infection, whereas it indicates that the KP onset is heterogeneous.
BACKGROUND: Killian polyp (KP) is a benign lesion that arises from the maxillary sinus. The etiology of KP is unknown. The aim of this study was to investigate the potential involvement of humanpapilloma- (HPV) and polyoma-viruses (HPyV) infections in the onset of KP. METHODS: DNA from antral (n = 14) and nasal (n = 14) KP fractions were analyzed for HPV and HPyV sequences, genotypes, viral DNA load and physical status along with expression of viral proteins and p16 cellular protein. RESULTS: The oncogenic HPV16 was detected in 3/14 (21.4%) antral KPs, whilst nasal KPs tested HPV-negative (0/14). The mean HPV16 DNA load was 4.65 ± 2.64 copy/104 cell. The whole HPV16 episomal genome was detected in one KP sample, whereas HPV16 DNA integration in two KPs. P16 mRNA level was lower in the KP sample carrying HPV16 episome than in KPs carrying integrated HPV16 and HPV- negative KPs (p< 0.001). None of the antral and nasal KP samples tested positive for HPyV DNA (0/28). CONCLUSIONS: A fraction of KP tested positive for the oncogenic HPV16. HPV16 detection in the KP antral portion may be consistent with HPV16infection derived from the maxillary sinus. HPV16 DNA integration represents a novel finding. Altogether, these data improve our knowledge on the association between KP and HPV infection, whereas it indicates that the KP onset is heterogeneous.
Entities:
Keywords:
Human papillomavirus; Infection; Killian polyp; Nasal polyps; Polyomavirus
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