A further relevant example from the production of poliovirus vaccine is provided by SV40, a polyomavirus which is an extremely common infection of macaques and rhesus monkeys (Shah and Nathanson, 1976) where it persists in the kidneys in a latent form without causing a cytopathic effect (Sweet and Hilleman, 1960) . This virus grows much more slowly than poliovirus and thus an infection might not be observed during the vaccine production. It is estimated that almost everybody who was vaccinated against poliovirus between 1954 and 1961 also recieved viable SV40 together with the poliovirus vaccine. This is true for the live attenuated as well as for the inactivated poliovaccine, because, in the first case, no inactivation step was applied and, in the second case, the formalin inactivation step was insufficient to inactivate SV40 (Sweet and Hilleman, 1960) . Whereas in the case of the live vaccine, the route by mouth is a poor route for infection with SV40 (Sweet and Hilleman, 1960) , others were injected with inactivated poliovaccine together with infectious SV40. A long-term follow-up study with a small number of individuals, as well as the observation that, in spite of the large number of vaccinees (10-30 millions of 98 millions who were vaccinated, or almost 90% of individuals under 20 yr in 1961 (Shah and Nathanson, 1976) ) which are believed to have received infectious SV40, showed no corresponding increase in related cancers (Shah and Nathanson, 1976) . It should be mentioned, however, that (i) DNA-sequences of SV40 have been detected in association with different human tumors and at an higher incidence in mesotheliomas (Horaud, 1997) , (ii) that SV40 isolated from primary monkey kidney cells by Sweet and Hilleman (1960) induced sarcomas in newborn hamsters (Eddy et al., 1961) , and (iii) that SV40 is oncogenic for laboratory rodents (Magrath, 1991) .