Objective To analyze how the infection of human papillomavirus 16（HPV16）affects expression of DNA polymerase β（DNA polB）with the aim of probing the mechanism of over-expression of DNA polB in human cancers.Methods Four fragments of human DNA polB promoter were amplified and constructed into luciferase reporter vector pGL-Basic

generating pGL-BP

pGL-BMH

pGL-BMS

and pGL-BAT constructs respectively

and co-transfected with HPV16 or HPV6 into Hep2 cells.Luciferase activity was assayed 48 hours after transfection.Semi-quantitative RT-PCR was used to measure mRNA expression of endogenous DNA polB.Immunohistochemistry and in situ hybridization were used to analyze DNA polB expression and HPV16 or HPV6 infection in 38 cases of cervical lesions respectively.Results With co-transfection of HPV16 and DNA polB promoter-driving reporters into Hep2 cells

pGL-BP reporter in full-length DNA polB promoter presented markedly elevated luciferase activities（P<0.05）.However

the other three mutant reporters:pGL-BMH

pGL-BMS

and pGL-BAT

generated no reporting activities in the presence of HPV16（P>0.05）.On the contrary

all of polB promoter reporters were little stimulated in co-transfection of HPV6（P>0.05）.The transfection of HPV16 could enhance the endogenous polB mRNA expression compared with that of HPV6（3.42 vs.0.80

P<0.05）.The DNA polB expression was found in 8 of 10 HPV16-positive cervical intraepithelial neoplasia grade III（CIN III）cases

while was only found in 3 of 11 HPV6-positive condyloma accuminatum cases

but was negative in all chronic cervicitis cases.The correlation of DNA polB expression with HPV16 infection in cervical lesions was significant（P<0.05）.Conclusions HPV16 is able to specifically stimulate the expression of DNA polB in human epithelial cells through interaction with the core upstream regulatory sequences of DNA polB promoter.Over-expression of DNA polB might be an explanation for the molecular mechanism underlying HPV-related human cancers.