The Journal of Experimental Medicine, Vol 106, 863-881,
Copyright, 1957, by The Rockefeller Institute for Medical Research New York
THE INFLUENCE OF CORTISONE ON EXPERIMENTAL VIRAL INFECTION
:
IV. NEGATION OF INTERFERENCE AS THE MECHANISM BY WHICH CORTISONE INDUCES INCREASED VIRUS YIELDS
Edwin D. Kilbourne M.D.1 and
With the Technical Assistance of Barbara Ann Pokorny
1 From the Division of Virus Research, Department of Public Health and Preventive Medicine, Cornell University Medical College, New York
The interference with viral synthesis which is induced by large quantities of non-infective influenza B virus is inhibited or negated with small quantities of cortisone and other C-21 steroids. The specificity of this effect is attested by the inactivity of 11-alpha hydroxy epimers of highly active compounds. Maximal activity in negation of interference is associated with the presence of oxygen at the C-11 position of the steroid molecule.
In view of the demonstration that negation of interference can occur, it is concluded that the phenomenon of multiplicity reactivation of non-infective virus is not primarily influenced by cortisone. Rather, it is suggested that the reactivation phenomenon is unmasked by cortisone through its inhibiting effect on the autointerference intrinsic in multiplicity infection.
If it is accepted that influenza virus infections in ovo are self-limited in part by viral autointerference, present evidence is consistent with the view that negation of this autointerference is the mechanism by which cortisone induces definitively increased yields of virus.
Submitted on August 1, 1957
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