Background:　Esophageal　carcinoma　(EC)　is　one　of　the　major　cancers　in　China.　In　1982,　Syrjanen　first　hypothesized　the　relationship　between　human　papillomavirus　(HPV)　infection　and　the　development　of　esophageal　cancer.　Since　then,　many　reports　in　the　field　have　supported　this　viewpoint.　This　study　investigated　the　etiological　relationship　between　HPV　infection　and　the　occurrence　of　esophageal　carcinoma　at　Tangshan　City　of　the　Hebei　province　in　China.　Methods:　189　samples　of　esophageal　carcinoma　patients　were　collected.　DNA　and　RNA　were　isolated　from　samples,　HPV　DNA　was　detected　by　polymerase　chain　reaction　(PCR)　using　My09/11　for　HPV　L1,　and　HPV16　was　determined　using　type-specific　primer　sets　for　HPV16　E6.　The　HPV16　integration　site　was　verified　by　amplification　of　papillomavirus　oncogene　transcripts,　and　HPV16　oncogene　transcript　products　were　ligated　to　the　pMD-18　T　vector　and　sequenced　to　confirm　the　physical　location　of　HPV16　integration.　Results:　168　HPV-positive　samples　were　detected　in　189　samples,　and　among　them　76　specimens　were　HPV16　positive.　Approximately　600　bp　of　the　HPV16　oncogene　transcript　were　detected　in　nine　esophageal　cancer　samples.　Sequence　analysis　revealed　that　HPV16　E7　integrated　into　human　chromosome　2　in　three　samples,　into　human　chromosome　5　in　one　sample,　into　human　chromosome　6　in　one　sample,　into　human　chromosome　8　in　two　samples,　and　into　human　chromosome　17　in　two　samples.　The　results　verified　that　the　integrated　HPV16　E7　in　five　samples　harbored　one　mutation　of　viral　DNA　compared　with　the　HPV16　sequence　provided　in　GenBank　(K02718).　Conclusions:　The　high　prevalence　of　HPV16　suggests　that　HPV16　may　play　an　etiological　role　in　the　development　of　esophageal　cancer.　The　integration　of　HPV16　into　host　cell　chromosomes　suggests　that　persistent　HPV　infection　is　key　for　esophageal　epithelial　cell　malignant　transformation　and　carcinogenesis.