Background/Aims:　To　investigate　the　etiology　of　esophageal　cancer　(EC)　related　with　human　papillomavirus　(HPV)　infection.　Materials　and　Methods:　Fresh　surgically　resected　tissue　samples　and　clinical　information　were　obtained　from　189　patients.　Genomic　DNA　was　extracted,　and　HPV　was　detected　using　polymerase　chain　reaction　(PCR)　with　HPV　L1　gene　primers　of　MY09/11;　HPV16　was　detected　using　HPV16　E6　type-specific　primer　sets.　Copies　of　HPV16　E2,　E6,　and　the　human　housekeeping　gene　beta-actin　were　tested　using　quantitative　PCR　to　analyze　the　relationship　between　HPV16　integration　and　esophageal　squamous　cell　carcinoma　and　the　relationship　between　the　HPV16　integration　status　and　clinical　information　of　patients.　Results:　Of　the　189　samples,　168　HPV-positive　samples　were　detected,　of　which　76　were　HPV16　positive.　Among　the　HPV16　positive　samples,　2　cases　(E2/E6　ratio＞1)　were　2.6%　(2/76)　purely　episomal,　65　(E2/E6　ratio　between　0　and　1)　were　85.6%　(65/76)　mixture　of　integrated　and　episomal,　and　9　(E2/E6　ratio=0)　were　11.8%　(9/76)　purely　integrated.　The　results　indicate　that　integration　of　HPV16　was　more　common　in　the　host　genome　than　in　the　episome　genome.　The　prevalence　rate　of　HPV16　integration　is　increasing　with　the　pathological　stage　progression　of　esophageal　carcinoma　(EC).　Conclusion:　A　high　prevalence　of　HPV16　suggested　that　HPV16　has　an　etiological　effect　on　the　progress　of　EC.　Integration　of　HPV16　is　more　common　than　episome　genome　in　the　host　cells,　indicating　that　continuous　HPV　infection　is　the　key　to　esophageal　epithelial　cell　malignant　conversion　and　canceration.