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From the Departments of Preventive Medicine and Medicine, University of Virginia School of Medicine, Charlottesville, Virginia
Abstract
A heat labile, sedimentable substance capable of inactivating Coxsackie B1 and B3 viruses has been demonstrated in noncultured mouse brain and in certain other murine and primate tissues. The tissue and age distribution of this factor appears, in general, to be correlated with the in vivo sites of multiplication of these viruses and with their virulence for newborn and adult mice. It has been postulated that this material in brain and other tissues is specific virus receptor-site and that the relative abundance of this substance in cells of various tissues is an important determinant of age and tissue specific susceptibility to these agents.
Sequential loss, with age, of adsorptive capacity of mouse brain for Coxsackie B1 virus was demonstrated in quantitative studies. Amount of tissue employed was rate limiting, but inoculum size was not critical. Cortisone treatment did not increase adsorptive activity of adult mouse brain for this virus. Adsorption of Coxsackie B1 and poliovirus by brain homogenates was temperature dependent, being more marked in the case of the former. Adsorption of poliovirus by noncultured, extraneural rhesus monkey tissues was confirmed; adsorption of Coxsackie B1 virus was limited to rhesus monkey cerebral cortex, cerebellum and liver. Brain weight-virus adsorption curves demonstrated about equal activity of rhesus monkey brain against both virulent and avirulent polioviruses but marked differences were observed in similar studies utilizing newborn mouse brain against virulent and avirulent strains of Coxsackie B3 virus.
These studies are presented as evidence that age specific susceptibility and mouse virulence of certain Coxsackie viruses are related to the relative abundance of receptor-like substance in host tissues.
Footnotes
1 This investigation was conducted under the sponsorship of the Commission on Acute Respiratory Diseases, Armed Forces Epidemiological Board, and was supported by the Office of the Surgeon General, Department of the Army.
A portion of this study was presented before the American Society for Clinical Investigation, May 1, 1961 (1).
2 John and Mary R. Markle Scholar in Medical Sciences.
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