A total of 513 women with cervical HPV infections have been followed-up since 1981 (mean 25.6 months) to establish the biological potential of HPV in cervical carcinogenesis. On each attendance, the patients were subjected to colposcopy accompanied by Papanicolaou (PAP) smears and/or punch biops1s The latter were analysed for mPV partlcles on TEM, for the cyto­pathic changes of HPV, as well as for HPV structural proteins. The local immunocompetent cell (ICC) infiltrates are enumerated using ANAE-technique to define B-, MPS- and T cells, and mo­noclonal antibodies for T cell subsets, NK and K cells and Langerhans cells. HPV DNA typing was accomplished by Southern blot and spot hybridization using the DNA probes for HPV 6, l1 16 and l8. Antibody titres for HSy were measured, and Chlamydia trachomatlS 1solations CO卢pleted m cervical swabs. No correlatlon with the clinical course, e.g. regression (RE)，per­sistence (EE)，progression (PR) or recurrence (RC) of the HPV lesions could be established for the following factors; expression of HPV antigens, presence of HPV particles on TEM, Chlamy­dia in cervical swabs, the levels of HSV antibodies, and the levels of the ICCs, The OKT4+ / OKTS+ cell rutio, however, was inversely correlated with PR, being most markedly reduced in recurrent lesions. Of the 513 lesions, 24.8% regressed, 59.8% remained persistent, and 14.1 % progressed, 11.9% having been coned due to progression into CIS. So far, 1.1 % of lesions have recurred after such a treatment. The progression rate was higest (45.5%) in HPV 16 le­sions, followed by that (27.3%) in HPV 18 lesions, as contrasted to 0% and 13.3% for HPV 6 and 11, respectively. The results clearly confirm that cervical HPV infections are capable of pro­gressing int9CIS and thus show a natural history equivalent to that of classical CIN. The inhe­rent potential of HPV 16 and HPV 18 lesions for clinical progression was clearly established, supporting the concept on HPV 16 and HPV 18 as the high risk HPV types in cervical carcino­genesis.