The Effect of Interferon on the Synthesis and Activity of an RNA Polymerase Isolated from Chick Cells Infected with Semliki Forest Virus

Sonnabend, Joseph; Martin, E. M.; Mécs, E.; Fantes, K. H.

doi:10.1099/0022-1317-1-1-41

Cited by 24 publications

(10 citation statements)

References 12 publications

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“…Thus, the inhibition of viral RNA synthesis could result from the primary inhibition of viral RNA polymerase synthesis Friedman and Sreevalsan, 1970). A similar depression of viral polymerase synthesis was found in Semliki Forest virus infection of chick cells Sonnabend et al, 1967) and in Mengovirus infection of L cells (Miner et al, 1966).…”

Section: Inhibition Of Viral Message Translation In Cells Extensive supporting

confidence: 53%

Antiviral activities of interferons

Stewart

Lin

1979

Pharmacology & Therapeutics

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Section: Inhibition Of Viral Message Translation In Cells Extensive supporting

confidence: 53%

Antiviral activities of interferons

Stewart

Lin

1979

Pharmacology & Therapeutics

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“…The results suggested that interferon blocks virus growth by inhibiting production by parental virus of the polymerase necessary for formation of the ribonuclease-resistant templates employed in the production of new viral RNA. This in turn suggested, in agreement with previous observations (1,9,10,13,16), that the mechanism for interferon action involves the inhibition of virus protein synthesis.…”

supporting

confidence: 91%

“…Levy, personal communication). In addition, during the log phase of virus growth, interferon treatment inhibits the formation of at least two virus specific proteins, the RNA polymerases of Mengo virus (13) and of Semliki forest virus (SFV) (16).…”

mentioning

confidence: 99%

Interferon Action on Parental Semliki Forest Virus Ribonucleic Acid

Friedman

Fantes

Levy

et al. 1967

J Virol

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Actinomycin D-treated chick fibroblasts were infected with purified 32P-labeled Semliki forest virus, and ribonucleic acid (RNA) was extracted after 1 or 2 hr. Within 1 hr, viral RNA forms sedimenting in sucrose gradients at 42S, 30S, and 16S were present. The 42S form corresponded to the RNA of the virion. The 16S form appeared to be a double-stranded template for the formation of new viral RNA, since nascent RNA was associated with it and the molecule could be heat-denatured and subsequently reannealed by slow cooling. Interferon treatment before infection, or puromycin (50 ,g/ml) or cycloheximide (200 ,g/ml) added at the time of virus infection, had no effect on the formation of the 30S RNA but inhibited the production of the 16S form. Several findings made it unlikely that these results were due to breakdown of parental RNA and reincorporation of 32P into progeny structures. The results suggested that the mechanism of interferon action involves inhibition of protein synthesis by parental viral RNA, since a specific viral RNA polymerase had previously been demonstrated to be necessary for production of 16S RNA. No protein synthesis appears necessary for formation of 30S RNA from parental virus RNA.on July 6, 2020 by guest

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“…Most of the studies with intact cells point to one of two processes as the primary targets of interferon action: (i) the transcription of early viral mRNA (2, 3, 14, 15, 25, 26, 33; M. N. Oxman, personal communication); and (ii) the translation of early viral mRNA (4,10,20,23,28,29,34,40). The inhibition of viral RNA synthesis in vitro has not yet been reported, only an accelerated degradation (27).…”

Section: Fig 1 Competition Between Mouse Globin Mrnamentioning

confidence: 99%

Interferon Treatment of Ehrlich Ascites Tumor Cells: Effects on Exogenous mRNA Translation and tRNA Inactivation in the Cell Extract

Sen

Gupta

Brown

et al. 1976

J Virol

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We reported earlier that in cell extracts that were prepared from interferontreated Ehrlich ascites tumor cells and preincubated and passed through Sephadex G-25 (S3OINT), the translation of exogenous mRNA (viral and host) was impaired and the impairment could be overcome to a large extent by adding a crude tRNA preparation from Ehrlich ascites tumor cells but not from Escherichia coli. We find now that the rate of inactivation of some tRNA's (especially those specific for leucine, lysine, and serine) but not those of many others is faster in S30INT than in corresponding extracts from control cells. This increased rate of tRNA inactivation may perhaps account for the need for added RNA to overcome at least partially the impairment of translation in S301NT. The relationship of the increased rate of tRNA inactivation to the antiviral effect of interferon is unclear. So far no significant difference has been detected in the amount of tRNA needed to overcome the impairment of encephalomyocarditis virus RNA translation in S301mr between tRNA from interferon-treated cells and tRNA from control cells. Furthermore, no difference was found in the rate of inactivation in S30INT between leucine-specific tRNA's from interferontreated and from control cells. tRNA's specific for leucine and lysine were not inactivated (unless very slowly) during incubation under our conditions in an extract from interferon-treated (or from control) cells unless the extract had been passed through Sephadex G-25 or dialyzed. The translation of exogenous mRNA was, however, impaired in an extract from interferon-treated cells that had not been passed through Sephadex G-25. overcome by added tRNA.

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The Effect of Interferon on the Synthesis and Activity of an RNA Polymerase Isolated from Chick Cells Infected with Semliki Forest Virus

Cited by 24 publications

References 12 publications

Antiviral activities of interferons

Antiviral activities of interferons

Interferon Action on Parental Semliki Forest Virus Ribonucleic Acid

Interferon Treatment of Ehrlich Ascites Tumor Cells: Effects on Exogenous mRNA Translation and tRNA Inactivation in the Cell Extract

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