Publication details
Epstein-Barr virus may contribute to the pathogenesis of adult-onset recurrent respiratory papillomatosis: A preliminary study
| Authors | |
|---|---|
| Year of publication | 2020 |
| Type | Article in Periodical |
| Magazine / Source | CLINICAL OTOLARYNGOLOGY |
| Citation | |
| Doi | http://dx.doi.org/10.1111/coa.13681 |
| Keywords | Epstein- Barr Virus Infections; Larynx Neoplasms; Papillomatosis; Papillomavirus Infections; Respiratory Tract Infections; Risk Factors |
| Description | Objective Human papillomavirus (HPV) causes adult-onset recurrent respiratory papillomatosis (AORRP), but AORPP prevalence is much lower than HPV prevalence. Thus, HPV infection is necessary, but not sufficient, to cause AORRP and other factors likely contribute to its pathogenesis. The present study aimed to investigate whether co-infection with herpetic viruses may contribute to the pathogenesis of AORRP. Design Prospective case-control study conducted from January 2018 to November 2019. Settings Tertiary referral centre. Participants Eighteen consecutive patients with AORRP and 18 adults with healthy laryngeal mucosa (control group) undergoing surgery. Main outcome measures Cytomegalovirus, Epstein-Barr virus (EBV), herpes simplex viruses 1 and 2, human herpesvirus 6, varicella zoster virus and HPV (including genotyping) were detected in biopsies of papilloma or healthy mucosa using real-time polymerase chain reaction and reverse line blot. Dysplasia and Ki67 levels were determined in papilloma specimens. Results EBV was present in 6 (33.3%) AORRP patients and no control patients (P = .019). Presence was not dependent on tobacco exposure (P = .413) or HPV genotype or concentration (P > .999). EBV presence was strongly related to increased cell proliferation (P = .005) and number of previous surgeries (P = .039), but not dysplasia (P > .999). Human herpesvirus 6 was found in 3 (16.7%) AORRP biopsies, with one false positive. No other herpetic virus was found. Conclusions Unlike other herpetic viruses, EBV seems to interact with HPV, enhancing cell proliferation and contributing to the pathogenesis and progression of AORRP. Further research is required to elucidate specific interactions and their role in the pathogenesis of AORRP. |