The reliable assessment of epidemiology of genital HPV infections is hampered by a number of technical problems. Until recently, methods based on morphological approaches played a central role in HPV diagnosis, i.e. macromorphology, colposcopy, cytology and histopathology, supplemented by immunohistochemical and DNA-hybridization techniques and most lately by DNA amplification with PCR. Because of the fact that these morphological techniques are extremely difficult to standardize, they are subject to major variations, both interobserver and intraobserver. Further confusion in the field is created by the biological behaviour of HPV infections. As established by the long-term prospective follow-up study run in Kuopio since 1981 and including over 500 women, clinical progression and regression were significantly related to grade of the lesion at the time of diagnosis (p less than 0.00001, and p = 0.0005, respectively), as well as to the type of HPV (p = 0.0012). Most importantly, however, genital HPV infections seem to run an extremely fluctuating course, a passage from a manifest to a subclinical or latent infection being frequently encountered in individual patients when examined at 6-month intervals for prolonged periods. This explains the significantly divergent prevalence figures reported in different series (ranging from 2% to 80%), which are completely dependent on the technique used to analyse the presence of HPV, i.e., whether (a) PAP smear, (b) biopsy, (c) DNA hybridization, or (d) PCR amplification. The first two are capable of disclosing only manifest (clinical) infections, the latter two also (at least theoretically) the subclinical and latent ones. In unselected Finnish female population at the age of 22 years, the prevalence of clinical (i.e. detectable by PAP smear) HPV infections was about 3%, and the adjusted annual incidence was 8.0%. According to the estimates for the life-time risk, up to 79% of the Finnish females would contract at least one HPV infection within ages 20 to 79 years. When related to the long-term trends in invasive cervical cancer in Finland (data available between 1953-1988), the figures indicate that this 79% life-time risk of getting HPV-infected or even the observed 15% of clinical progression rate for HPV infections in the prospective follow-up study by no means signify an identical risk for development of cervical cancer (i.e. 0.79 X 0.15 = 11%). It seems likely that in countries where mass-screening programmes exist (and precancer lesions are traced and eradicated), the high prevalence of HPV infections is not necessarily reflected as increased prevalence figures of invasive cervical carcinomas.(ABSTRACT TRUNCATED AT 400 WORDS)