The incidence of ENT tumors (benign and malignant) is increasing worldwide . This study reports a general frequency of 17.5% cases of benign and malignant ENT tumor per year in Ouagadougou. Generaly, in Burkina Faso, the ENT pathology remains dominated by infections followed by tumors, trauma and malformations. However in recent years, cases of benign and malignant tumors are more and more frequent . In Tunisia, Charfi et al., report 26 cases of inverted nasosinus papilloma over 11 years .
Etioepidemiology of cases of ENT tumors histologically diagnosed between 2007-2017
In ENT tumors, the main risk factors are tobacco, alcohol and viruses. In fact smokers are 2.7 times more likely to contract HPV than people who have never smoked. For heavy smokers who smoke at least 20 packs of cigarettes per year, the probability of acquiring HPV is more than three times higher than for non-smokers during their lifetime . Others say positive HPV oropharyngeal cancers are less common in smokers than in heavy drinkers [17, 18]. In general, HPV has a tropism for the epithelial cells of the skin and mucous membranes but can survive freely in the environment for several months, which contributes considerably to its virulence. People with oral cancer due to HPV have higher survival rates  than those with others risks factors. The emergence of an oral squamous cell linked to HPV significantly improves the overall survival rates at 5 years in primary squamous cell carcinomas of the base of the tongue (from 25% to 51%) and tonsils (of 28% to 61%).This is independent of the stage at diagnosis and the methods of treatment, compared to oral cancers attributed to smoking and alcohol consumption. Oral HPV infection is most commonly associated with oral mucosal disease  although associations have also been observed with pulp disease  and periodontal [22, 23]. These authors report that HPV infection plays a causal role in various clinical presentations of oral warts such as squamous papilloma, genital warts, common wart and focal epithelial hyperplasia[24–26]. American studies report a prevalence of 2 to 3% of oral warts in adults infected with HIV. These adults were on antiretroviral therapy [27, 28]. This rate is considerably higher than the estimated prevalence of less than 0.5% in the general population[29–31].
This study reports a predominant male prevalence at 1.69%. Other authors have reported similar results. In fact, Sander et al report that the prevalence of HPV by sex is dependent on the type of population . On the other hand, Kreimer et al found any statistically significant difference in the ENT prevalence of HPV by gender .
All ages are affected by positive ENT-HPV tumors and the relationship between age and detection of HPV is not linear. In this study, the youngest was 04 months old and the oldest 80 years old. Several authors have reported the same results in Ouagadougou (17,6%). With some authors, adults aged 55 to 64 were twice as likely to contract HPV as those aged 18 to 24 . These results are consistent with other studies reporting a non-significant increase in the age-related ENT prevalence of HPV in age groups ranging from 18 to 24 and 55 to 74 (Kreimer et al. 2011). However, according to Marais et al., the prevalence of oncogenic types of cervical HPV decreased with age, compared to other types of non-oncogenic HPV .
Prevalence of HPV infection in ENT tumors
This first study of its kind in Burkina Faso reports a general prevalence of 37.7% (66/175) of HPV in ENT tumors. In general, the prevalence of LR-HPV (54.55%, 36/66) was higher than that of HR-HPV (25.76%, 17/66). In Burkina Faso, Djigma et al., reported a high prevalence of HPV infection in HIV + women compared to HIV. Among these authors, the prevalence of HPV was 25.4% in HIV-negative women and 59.0% in HIV-positive women (p <0.01). However, these authors have worked on cervical specimens. A meta-analysis conducted in 1997 assessing the prevalence of HPV in oral tissues and cells reported increasing prevalence rates of HPV in benign lesions of the malignant tumor. In this meta-analysis, the probability of detecting HPV in normal oral mucosa was 10.0%, significantly less than in benign leukoplakia (22.2%), intraepithelial neoplasia (26.2%), carcinomas warty (29.5%) and oral squamous cell carcinoma (46.5%) .Of the 14 HR-HPV genotypes tested in this study, 9 genotypes were identified as well as both of the LR-HPV genotypes sought. Considering the types of HPV in isolated infections, the HPV56 genotype had the highest prevalence (47%, 8/17) followed by HPV33 (17.6%, 3/17). The each other types of HR-HPV gave a prevalence of 5.9% (1/17). The absence of other HR-HPV genotypes in this study is likely due to the assay kit used. Other authors , having worked on 37 types of oral HPV, 36 types have been detected. The oncogenic type HPV-16 was most common in 1.1% of the participants. HPV 62, 55 and 66 were found in more than 0.5%. These differences with the results of this study could be explained by the type of kit used which does not allow a large number of genotypes to be determined as well as the age of the samples which does not allow a better extraction of DNA. These authors worked on freshly collected oral samples. The cross-sectional and retrospective concept of this study was necessary to achieve the objectives of estimating the prevalence and genotyping of HPV in ENT tumors. However, cross-sectional and retrospective observations impose significant limits on the interpretation of the results. For example, the representativeness of the sample in relation to the general population. Evidence that the persistence of HPV infection is important for the etiology of cervical cancer [36, 37] would probably be valid for carcinogenesis of the oropharynx.
In the case of LR-HPV, the predominant genotype in this retrospective study was HPV6 with a prevalence of 55% (20/36).
For some authors, the types of HPV most commonly associated with genital warts, genital papillomas and oral benign are HPV 6 and 11[25, 38]. Oral warts, less common, presenting as focal epithelial hyperplasia. These oral warts are caused by HPV types 13, 32, 2 and 4 . The mode of HPV transmission, the person's age and immunity, as well as the many sexual practices, would probably explain these differences in the results [39, 40].
In the present study, multiple infections accounted for 19.7% (13/66) of the HPV positive samples. Among these samples, the co-infections between HPV-HR and HPV-LR were predominant with a rate of 46.14% (6/13) and the co-infection HPV6 / 11 was 38.48%. Omland et al., reported in Norway a 7.2% distribution of HPV6-11 co-infection . In general, co-infection between the different types of HPV is frequent and an HPV infection can be associated with HR-HPV and LR-HPV. In this study the LR-HPV genotypes (HPV6 at 20/66 and HPV11 at 16/66) were predominant compared to HR-HPV (HPV 56 at 8/66). This difference could be explained by the fact that benign tumors are the most frequent compared to malignant tumors, depending on the location. In general, the pathologies associated with HPV in humans vary depending on the genotype involved. Oncogenic LR-HPV is not associated with the development of cancer, but malignant transformation can occur if the pathology is also associated with HR-HPV.
HPV infections are transient, most regress between 1 year and 18 months; but 10 to 20% persists, thus the development of a tumor. ENT transmission of HPV infections can be vertical oro-sexual . According to the figure 1, the genotypes of the nonavalent vaccine (HPV6/HPV11/HPV16/HPV18/31/33/45/52/58) showed a high prevalence (83,02%) followed by the genotypes of the quadrivalent vaccine (71,68%), and finally those of the bivalent vaccine (3,76%.) The prevalence of HPV35; 39; 51; 56 ; 59 ; 66 and 68 genotypes not covered by the three vaccines types was 16.98%. However HPV types 16 and 18 are responsible for 30 to 40% of cancers of the oropharynx according to WHO/ICO Information Centre on HPV and Cervical Cancer, 2010. Depending on the type of lesion and the location, different types of treatment are recommended, including surgical excision. However, no therapeutic method allows the eradication of the virus. This explains the fact that the virus can persist in the lesion area. It is therefore crucial to focus on hygiene and vaccination in the fight against HPV induced ENT tumors. The nonavalent vaccine is directed against HPV 6, 11, 16, 18, 31, 33, 45, 52 and 58. It covers 6 genotypes of HR-HPV and the two genotypes of LR-HPV encountered in our study. Vaccination with nonavalent could prevent HPV induced ENT- cancers. Prevention by vaccination is therefore very useful in combating ORL-HPV induced cancers.