Reactivation of Non-Infective Virus in a Cortisone-Injected Host

Abstract

The administration of cortisone to chick embryos inoculated with large quantities of inactive influenza B virus results in a rate of viral increase greater than is concommittantly observed with inocula of comparable infectivity which are devoid of inactive particles. Thus, more than a mere negation of autointerference is effected. It is concluded that in the presence of cortisone reactivation has occurred of non-infective virus to a state in which it can participate in viral synthesis. Cortisone-induced viral reactivation is dependent upon a high partide/cell ratio and is thus analogous to the previously described phenomenon of "multiplicity reactivation." Cortisone does not influence either homologous or heterologous viral interference unless reactivation of the inactive interfering virus occurs. Virus reactivable with cortisone possesses both interfering and enzymatic properties. Reactivation of virus with cortisone cannot be effected in vitro but is mediated by the host cell. Two hypotheses concerning the action of cortisone are presented.

The Influence of Cortisone on Experimental Viral Infection

“…) is an efficient method for destruction of infectivity and preservation of interfering capacity (5). These findings have been amply confirmed and extended by the present investigator and a thermal inactivation gradient of activities associated with the virus particle has been presented (2). In succession, infectivity, the capacity to participate in multiplicity reactivation, interfering capacity, eluting (enzymatic) function, and lastly, hemagglutinating capacity are destroyed by thermal stress.…”

“…The results of two such experiments (Experiments 90, 112) are set forth in Fig. 1, together with data from an earlier publication (2) in which multiplicity reactivation of non-infective virus was described. In Experiment 90 ( Fig.…”

“…This conclusion derived from evidence that final yields of virus were not enhanced with inactivated virus unless inactive virus capable of multiplicity reactivation was present (2). However, because observation of the early period of viral increase was essential to demonstration of the accelerated incremental rate occasioned by reactivation, measurements of viral yields in later time periods were seldom made.…”

“…compared with lower temperatures probably reflects some reactivation of virus rendered non-infective at 22-30°C. (2). In the studies presented here, inactivation temperatures of 22, 30, or 35°C.…”

“…Partial degradation of the virus particle by ultraviolet irradiation (3,4), heat (5,2) or sulfur mustard (6), destroys the ability of the particle to induce virus synthesis (infective property) but leaves it with its hemagglutinating capacity (by which it may be identified) and its capacity to block or interfere with virus synthesis induced by infective particles. Horsfall has shown that mild heat (22-35°C.…”