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R. A. JOSKE, MD, FRACP; D. D. KEALL, MA, MB, MRCP; P. J. LEAK, BSc; N. F. STANLEY, DSc; M. N. I. WALTERS, MB, MRACP

Arch Intern Med. 1964;113(6):811-816.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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, 2 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 . . . [Full Text PDF of this Article]

Author Affiliations
PERTH, WESTERN AUSTRALIA

Reader in Experimental Medicine, University of Western Australia (Dr. Joske); Physician, Princess Margaret Hospital for Children and Royal Perth Hospital (Dr. Keall); Research Assistant, Department of Microbiology, University of Western Australia (Miss Leak); Professor of Microbiology, University of Western Australia (Dr. Stanley); Senior Lecturer in Pathology, University of Western Australia (Dr. Walters).

From the School of Medicine, University of Western Australia.

Footnotes
Received for publication Oct 3, 1963; accepted Nov 15.

Supported in part by US Public Health Service research grant No. AI-04627-02 from the National Institutes of Health, and in part by the University of Western Australia.

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