Human papillomavirus (HPV) as a group of double stranded small DNA viruses, HPV infection is believed to be related with the development of many types of human tumors. Since the first report suggested that there was a close relationship between HPV infection and the pathologic change of esophageal squamous cell carcinoma (ESCC) by Syrjanen in 1982, a great amount of literatures had been published by scholars in this field in the past few decades. However, it is still controversial whether HPV infection plays a causal role in pathogenesis of esophageal carcinoma. Chaozhou-Shantou region is the only coastal area with a high incidence of esophageal carcinoma in Guangdong province in China. Previous studies have shown that there were high frequency of HPV infection in the samples of esophageal carcinoma and its paired adjacent tissues, indicating that HPV infection act an essential role in carcinogenesis of esophagus in this area. In order to further explore the present situation and the role of HPV (especially the high-risk HPV subtypes) infection in pathogenesis of esophageal carcinoma, nest-PCR was carried out to detect the infection and integration of HPV DNA in esophageal tissues with malignant lesions and normal tissues control, analyze its relationship between and the clinico-pathological characteristics of esophageal carcinoma with statistical methods, and assay for HPV genotyping by sequencing technique.Our research showed that: (1) The positive rates of HPV DNA in tumor, tumor-adjacent normal tissues and normal control mucosa of the esophagus were 77.36% (82/106), 80.19% (84/106) and 33.00% (33/100), respectively. Statistical analysis showed that the detection rates of HPV DNA in cases with esophageal carcinoma (EC) and tumor-adjacent were both significantly higher than those of normal control groups (P <0.01). But there was no difference in tumor-adjacent normal tissues and normal control mucosa of the esophagus (P >0.05); (2) HPV infection mainly existed in EC patients in ages from 35 to 47 years with a tendency that the positive rates of HPV infection decreased with the increase of ages of EC patients. And the HPV positive rates in smoking EC patients was 3.27 times higher than those nonsmoking patients (84.91% VS 67.35%,P<0.05,OR=3.27). However, they were not correlated with the gender, alcohol, tumor grade and lymph node metastasis of EC patients; (3) The distribution of HPV subtypes in esophageal carcinoma were as follows (from high to low): HPV-16 (62.6%), -58 (13.1%), -18 (11.1%), -33 (3.0%), -31 (3.0%) and -11 (1.0%). Multiple HPV genotypes infection included HPV-16/-18 and HPV-16/-33. And the HPV-16/-18 were the predominant multiple infection in esophageal carcinoma tissues (5.2%); (4) The integration rates of high risk HPV-16 DNA were 93.44% (57/61) in tumors, 50.85% (30/59) in tumor-adjacent tissues and 45.45% (10/22) in normal mucosa of the esophagus, respectively. Statistical analysis showed that the integration rates of HPV-16 DNA in cases with esophageal carcinoma were significantly higher than those of tumor-adjacent and normal control groups (P <0.01).Our results further demonstrated that:â‘ HPV infection was both frequently presented in tissues of esophagus from patients with esophageal carcinoma and normal persons. HPV mainly infected EC patients in ages raging from 35 to 47 years. Smoking and age were the risk factors of HPV infection in esophageal carcinoma.â‘¡High-risk HPV subtypes, particularly HPV-16, -58 and -18 prevalence dominantly existed in cancerous tissues.â‘¢There were high prevalence of HPV-16 DNA integrating into the host cells in malignant transformation of esophageal carcinoma, and it might be play an important role in esophagus carcinogenesis. |