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Association between oncogenic human papillomavirus type 16 and Killian polyp
Lucia Oton-Gonzalez1, John Charles Rotondo1, Luca Cerritelli2
1Department 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.
Infectious Agents and Cancer
|January 8, 2021
Summary
The oncogenic human papillomavirus type 16 (HPV16) was detected in Killian polyp (KP) tissue, suggesting a potential role for HPV in the heterogeneous etiology of this benign maxillary sinus lesion. HPV16 DNA integration was also observed.
Area of Science:
- Otolaryngology
- Virology
- Pathology
Background:
- Killian polyps (KP) are benign maxillary sinus lesions with unknown etiology.
- Investigating viral involvement, specifically human papillomavirus (HPV) and polyomavirus (HPyV), is crucial for understanding KP pathogenesis.
Purpose of the Study:
- To investigate the potential role of HPV and HPyV infections in the development of Killian polyps.
- To analyze viral sequences, genotypes, DNA load, and physical status in KP samples.
Main Methods:
- DNA analysis of antral and nasal KP fractions for HPV and HPyV.
- Quantification of viral DNA load and assessment of physical status (episomal vs. integrated).
- Evaluation of viral protein and p16 cellular protein expression.
Main Results:
- The oncogenic HPV16 was detected in 21.4% of antral KPs, but not in nasal KPs.
- HPV16 DNA load averaged 4.65 ± 2.64 copies/10^4 cells, with episomal and integrated forms identified.
- No HPyV DNA was detected in any KP samples.
Conclusions:
- A subset of Killian polyps harbors HPV16, particularly in the antral portion, suggesting maxillary sinus origin.
- HPV16 DNA integration is a novel finding in KP.
- These findings indicate a heterogeneous etiology for Killian polyps, with HPV infection being a contributing factor in some cases.
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