The Influence of Cortisone on Experimental Viral Infection

Ed, Kilbourne

doi:10.1084/jem.106.6.883

Cited by 17 publications

(10 citation statements)

References 13 publications

(13 reference statements)

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“…Titers have not been related to membrane wet or dry weights because of the primary concern with measuring the total vires/egg. The growth-inhibiting action of cortisone (9) would necessitate possibly misleading "correction" of titration values if hemagglutinin yields were related to weight units. Because all membranes are diluted similarly, it was deemed equally useless to recalculate titers on the basis of volume.…”

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The Influence of Cortisone on Experimental Viral Infection

1957

The Journal of Experimental Medicine

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Earlier publications have presented evidence that the course of influenza virus infection in chicken embryos, mice, and tissue culture is strikingly affected by the administration of corticosteroid hormones. It has been shown that under appropriate experimental conditions final yields of virus are increased (1-3), that antibody formation, acquired immunity (4), and inflammatory reaction (3) are depressed, that the survival time of infected chicken embryos is prolonged (3), and that "multiplicity reactivation" of non-infective virus is clearly demonstrable (5).Ensuing studies have clarified the mechanisms of cortisone action in the influenza virus-chicken embryo system. The results of these studies are presented in this and two companion papers. It will be demonstrated that cortisone and related steroids have two distinct effects on the course of influenza virus multiplication: (a) inhibition of viral synthesis, and (b) inhibition of the autointerference caused by large numbers of viral particles. Yields of virus will be shown to be the resultant of these two contrasting effects.The present paper is concerned with the influence of cortisone on the dynamics of influenza virus increase. It will be evident that consideration of these kinetics has been essential in defining the mechanisms of cortisone action. Materials and MethodsViruses.--The Lee strain of influenza B virus and the PR8 strain of influenza A virus were used as allantoic fluid suspensions. Dilutions of virus were made in 0.01 M phosphate buffered NaC1 (0.85 per cent) solution. To "inactive" viral inocula derived from thermally inactivated virus were added streptomycin (1 mg./ml.) and penicillin (100 units/ml.). Preparations designated as "active" virus were prepared as suggested by Horsfall (6, 7) to contain a relatively high proportion of infective viral particles (see Kilbourne (5)). Viruses were stored at --68°C. in a special CO~ box in which CO2 is excluded from the specimen compartment (8). RDE *

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The Influence of Cortisone on Experimental Viral Infection

1957

The Journal of Experimental Medicine

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“…(a) Ribonudease, which inhibits the synthesis of influenza viruses in the egg (14) (as does cortisone (1,15)), has been found in this laboratory not to inhibit interference.…”

Section: The Mechanism By Which C-z1 Steroids Fnduce Negation Of Viramentioning

confidence: 89%

“…(b) Measurement of dry weights of embryos from eggs injected with as little as lpg. of cortisone has revealed inhibition of weight gain (15). As the depressing effects of glucocorticoids on protein synthesis (17) and cellular proliferation (18) of viral interference may be related to either of these effects.…”

Section: The Mechanism By Which C-z1 Steroids Fnduce Negation Of Viramentioning

confidence: 99%

The Influence of Cortisone on Experimental Viral Infection

1957

The Journal of Experimental Medicine

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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.

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“…Although earlier studies have demonstrated the marked influence of cortisone on the multiplication of influenza B virus ( 1 1, 12), significant effects on multiplication of 1302 virus have not been shown. In contrast, studies with unadapted influenza B virus in mice have demonstrated the selection on passage of virus partially "dependent" on cortisone for both multiplication and pathogenicity (13). However, only the cardio-pathogenic effects of 1302 virus may be described as cortisone-dependent.…”

Section: Discussionmentioning

confidence: 99%