Is poliomyelitis a genetically-determined disease? I: A genetic model

Abstract

Previous work suggesting genetic susceptibility to paralytic poliomyelitis is reviewed and previous explanations of the high attack rate at Chesterfield Inlet, 1948, are rejected as incompatible with other data. The case-fatality rate in many epidemics is interpreted as showing two different populations of those attacked. A model of genetic susceptibility is proposed in which susceptibility to paralytic poliomyelitis is inherited as a single gene (p +) and that homozygotes (p +p +) become susceptible soon after birth whereas heterozygotes (p +p −) do not become susceptible till a later age. The over-riding role of immunity is discussed. The Hardy-Weinberg formula is used to analyse the New York Epidemic 1916 and the Chesterfield Inlet Epidemic among Eskimos in 1948: the case-rates of paralytic poliomyelitis are shown to be compatible with the model and the populations to be genetically similar. Clinical aspects of the disease are reassessed and unified by the model. The role of other genes affecting susceptibility is discussed.