Enterovirus immunity and the hygiene hypothesis

Abstract

The current knowledge fits with a scenario where one or more commonly circulating enteroviruses initiate the beta-cell damaging process in early childhood. These viruses may represent certain enterovirus types and strains which have special properties explaining their ability to cause beta-cell damage (e.g., tropism to islet cells). Particular susceptibility for the virus is probably needed and only a small fraction of infected individuals may develop beta-cell damage. In this sense type 1 diabetes has many similarities with polio, the well-known enterovirus disease. Based on experience from polio, both the increasing incidence of type 1 diabetes and the remarkable geographical variation in the incidence rates can be related to varying circulation of diabetogenic enteroviruses in these populations. On the hand, animal experiments have suggested that under certain conditions enteroviruses may also have a protective effect, which seem to be mediated by their ability to activate immunoregulatory mechanisms. Both these aspects (risk vs. protective effect) should be taken into account when possible viral effects on the epidemiology of type 1 diabetes are investigated. Large-scale birth cohort studies, such as the TEDDY study, will play a key role in the identification of these effects and virus-host interactions which determine the outcome of the infection.