1[1]World Health Organization.The World Health Report 2004.Geneva.2001,37(2):246～250.
2[2]Andersson S,Rylander E,Larsson B,et al.The role of human papillomavirus in cervical adenocarcinoma carcinogenesis:Eur J Cancer,2001,37(2):246～250.
3[3]Zur Hausen H.Papillomaviruses in human cancers.Proc Assoc Am Physicians,1999,111(6):581～587.
4[4]Zur Hausen H.Papillomaviruses and cancer:from basic studies to clinical application.Nat Rev Cancer,2002,2(5):342～350.
5[5]Youde SJ,Dunbar PR,Evans EM,et al.Use of fluorogenic histocompatibility leukocyte antigen-A·0201/HPV 16 E7 peptide complexes to isolate rare human cytotoxic T-lymphocyte-recognizing endogenous human papillomavirus antigens.Cancer Res,2000,60(2):365～371.
6[6]Evans EM,Man S,Evans AS,et al.Infiltration of cervical cancer tissue with human papillomavirus-specific cytotoxic T-lymphocytes.Cancer Res,1997,57(14):2 943～2 950.
7[7]Frazer IH.Prevention of cervical cancer through papillomavirus vaccination.Nat Rev Immunol,2004,4(1):46～54.
8[8]Carter JJ,Koutsky LA,Hughes JP,et al.Comparison of human papillomavirus types 16,18,and 6 capsid antibody responses following incident infection.J Infect Dis,2000,181(6):1 911～1 919.
9[9]Viscidi RP,Schiffman M,Hildesheim A,et al.Seroreactivity to human papillomavirus (HPV) types 16,18,or 31 and risk of subsequent HPV infection:results from a population-based study in Costa Rica.Cancer Epidemiol Biomarkers Prev,2004,13(2):324～327.
10[10]Frazer IH,Thomas R,Zhou J,et al.Potential strategies utilised by papillomavirus to evade host immunity.Immunol Rev,1999,168:131～142.
