Prevalence of human papilloma virus and human herpes virus types 1–7 in human nasal polyposis

✍ Scribed by Apostolos Zaravinos; John Bizakis; Demetrios A. Spandidos

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 110 KB
• Volume: 81
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.21534

✦ Synopsis

Abstract

This study aimed to investigate the prevalence of human papilloma virus (HPV), herpes simplex virus‐1/‐2 (HSV‐1/‐2), varicella‐zoster virus (VZV), Epstein–Barr virus (EBV), cytomegalovirus (CMV), and human herpes virus‐6/‐7 (HHV‐6/‐7) in 23 human nasal polyps by applying PCR. Two types of control tissues were used: adjacent inferior/middle turbinates from the patients and inferior/middle turbinates from 13 patients undergoing nasal corrective surgery. EBV was the virus most frequently detected (35%), followed by HPV (13%), HSV‐1 (9%), and CMV (4%). The CMV‐positive polyp was simultaneously positive for HSV‐1. HPV was also detected in the adjacent turbinates (4%) and the adjacent middle turbinate (4%) of one of the HPV‐positive patients. EBV, HSV, and CMV were not detected in the adjacent turbinates of the EBV‐, HSV‐ or CMV‐positive patients. All mucosae were negative for the VZV, HHV‐6, and HHV‐7. This is the first study to deal with the involvement of a comparable group of viruses in human nasal polyposis. The findings support the theory that the presence of viral EBV markedly influences the pathogenesis of these benign nasal tumors. The low incidence of HPV detected confirms the hypothesis that HPV is correlated with infectious mucosal lesions to a lesser extent than it is with proliferative lesions, such as inverted papilloma. The low incidence of HSV‐1 and CMV confirms that these two herpes viruses may play a minor role in the development of nasal polyposis. Double infection with HSV‐1 and CMV may also play a minor, though causative, role in nasal polyp development. VZV and HHV‐6/‐7 do not appear to be involved in the pathogenesis of these mucosal lesions. J. Med. Virol. 81:1613–1619, 2009. © 2009 Wiley‐Liss, Inc.