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April 22, 1950


Author Affiliations

Philadelphia; Boston; Philadelphia

From the Municipal Hospital, Camden, N. J. (Drs. Coriell and Murphy) and from the Children's Hospital of Philadelphia (Department of Pediatrics, University of Pennsylvania School of Medicine), Philadelphia (Drs. Coriell, Murphy and Stokes); from the Division of Clinical Laboratories, Children's Hospital, and the Department of Pediatrics, Harvard Medical School, Boston (Dr. Siegel), and from the Department of Pediatrics, Children's Medical Center, Harvard Medical School (Dr. Cook).

JAMA. 1950;142(16):1279-1281. doi:10.1001/jama.1950.02910340025007

Certain data about poliomyelitis suggest an unusual host-parasite relationship. Among these are the low incidence of paralysis,1 less than 1 in 100 cases of poliomyelitis infection; the familial incidence,2 constitutional factors3 and endocrine imbalance theories4 which have been advanced to explain susceptibility; excessive fatigue and chilling or exhaustion during the incubation period, which is frequently followed by severe paralysis, and the greater incidence of paralysis in pregnant women as compared with nonpregnant women.5 The concept of latent immunization to various antigenic types of virus does not explain the epidemiologic patterns of the disease.6 All these observations suggest that susceptibility or resistance to poliomyelitis involves nonspecific defensive mechanisms and, indirectly, that the host response is more important than the virulence of the virus in determining the course of infection. Rapid mobilization of bodily defensive mechanisms may limit the spread of infection in the usual nonparalytic