The role of the reoviruses in human disease remains speculative. The initial isolation of the prototype reovirus 3 (hepatoencephalomyelitis virus—HEV) by Stanley et al1 was from the stools of an Australian aboriginal child, 2½ years of age, who was suffering from bronchiectasis and bronchopneumonia as well as patchy alopecia and conjunctivitis. Four years later, van Tongeren2 isolated a similar virus from the stool of a Dutch child with convulsions. In neither case was it possible to establish an etiological relation between the virus and the clinical condition of the child.
Since these early studies, the problem of possible human pathogenicity of reoviruses has been pursued both experimentally and clinically.
All three serotypes have been shown to cause antibody production in a large variety of domestic and laboratory animals, but gross pathological changes are known to occur only in infant mice. These have been studied in considerable detail3
JOSKE RA, KEALL DD, LEAK PJ, STANLEY NF, WALTERS MNI. Hepatitis-Encephalitis In Humans With Reovirus Infection. Arch Intern Med. 1964;113(6):811–816. doi:10.1001/archinte.1964.00280120011003
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