Herberhold Stephan, Hellmich Martin, Panning Marcus, Bartok Eva, Silling Steffi, Akgül Baki, Wieland Ulrike
ENT Department, Head and Neck Surgery, University of Bonn, Bonn, Germany.
ENT Department, Johanniter-Kliniken Bonn, Bonn, Germany.
Med Microbiol Immunol. 2017 Apr;206(2):93-103. doi: 10.1007/s00430-016-0486-6. Epub 2016 Nov 10.
Human papillomaviruses (HPVs) are an acknowledged cause of a subset of oropharyngeal cancers, especially of tonsillar cancer. Similar to HPV, some human polyomaviruses (HPyVs), such as Merkel cell polyomavirus (MCPyV), have an oncogenic potential. Recently, several novel HPyVs have been discovered. The aim of our study was to determine viral DNA prevalence and viral DNA load of 13 different HPyVs in benign and malignant tonsillar tissue and to compare the data with those found for HPV. A total of 78 biopsies of palatine tonsils with a histologic diagnosis of non-malignant disease (chronic tonsillitis, tonsillar hyperplasia, n = 40) or tonsillar squamous cell carcinoma (n = 38) were included in the study. HPyV DNA prevalence and viral load were determined by virus-specific quantitative real-time PCRs. JCPyV (1/40, 2.5%) and WUPyV (3/40, 7.5%) were only found in non-malignant tonsillar tissue. HPyV7 and HPyV10 were only detected in one (2.6%) and seven (18.4%) of the 38 cancer biopsies, respectively. Both MCPyV (8/38, 21.1 vs. 4/40, 10.0%) and HPyV6 (2/38, 5.3 vs. 1/40, 2.5%) were found more frequently in cancer samples than in non-malignant tissue, but the differences were not significant. BKPyV, KIPyV, TSPyV, HPyV9, STLPyV, HPyV12 and NJPyV were not discovered in any of the samples. HPyV loads found in HPyV DNA-positive biopsies were very low with no difference between non-malignant and malignant samples (median load <0.0001 HPyV DNA copies per beta-globin gene copy, respectively). In contrast to HPyV, high-risk HPV types (HPV16/HPV18) were found significantly more frequently in tonsillar cancers than in non-malignant tonsillar tissue (17/38, 44.7 vs. 2/40, 5.0%, p < 0.001). Furthermore, high-risk HPV DNA loads were significantly higher in the cancer compared to the non-malignant samples (median load 11.861 vs. 7 × 10 HPV DNA copies per beta-globin gene copy, p = 0.012). While both HPV and HPyV may persist in tonsillar tissue, our data on HPyV DNA prevalence and load do not support a role of HPyV in tonsillar carcinogenesis, neither alone nor as co-infecting agents of HPV.
人乳头瘤病毒（HPV）是口咽癌（尤其是扁桃体癌）一部分病例的公认病因。与HPV相似，一些人多瘤病毒（HPyV），如默克尔细胞多瘤病毒（MCPyV），具有致癌潜力。最近，发现了几种新型HPyV。我们研究的目的是确定13种不同HPyV在良性和恶性扁桃体组织中的病毒DNA流行率和病毒DNA载量，并将数据与HPV的相关数据进行比较。该研究共纳入78例腭扁桃体活检样本，其组织学诊断为非恶性疾病（慢性扁桃体炎、扁桃体增生，n = 40）或扁桃体鳞状细胞癌（n = 38）。通过病毒特异性定量实时PCR测定HPyV DNA流行率和病毒载量。JCPyV（1/40，2.5%）和WUPyV（3/40，7.5%）仅在非恶性扁桃体组织中发现。HPyV7和HPyV10分别仅在38例癌症活检样本中的1例（2.6%）和7例（18.4%）中检测到。MCPyV（8/38，21.1%对4/40，10.0%）和HPyV6（2/38，5.3%对1/40，2.5%）在癌症样本中的发现频率均高于非恶性组织，但差异不显著。BKPyV、KIPyV、TSPyV、HPyV9、STLPyV、HPyV12和NJPyV在任何样本中均未发现。在HPyV DNA阳性活检样本中发现的HPyV载量非常低，非恶性和恶性样本之间无差异（每β-珠蛋白基因拷贝的中位载量分别<0.0001个HPyV DNA拷贝）。与HPyV相反，高危HPV类型（HPV16/HPV18）在扁桃体癌中的发现频率显著高于非恶性扁桃体组织（17/38，44.7%对2/40，5.0%，p<0.001）。此外，癌症样本中的高危HPV DNA载量显著高于非恶性样本（每β-珠蛋白基因拷贝的中位载量为11.861对7×10个HPV DNA拷贝，p = 0.012）。虽然HPV和HPyV都可能在扁桃体组织中持续存在，但我们关于HPyV DNA流行率和载量的数据不支持HPyV在扁桃体致癌过程中发挥作用，无论是单独作用还是作为HPV的共同感染因子。
