RNA‐Induced Interference with Animal Virus Infection

Matsuyama, M; Kawade, Yoshimi; Fukada, Takashi

doi:10.1111/j.1348-0421.1970.tb00528.x

Cited by 4 publications

(2 citation statements)

References 7 publications

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“…In our studies on RNA-induced interference [10,19], protamine was almost always included in the RNA-containing medium, since it was found to greatly enhance the action of inducer RNA. In our experiments previously reported on the antagonism of non-inducer RNA [16], the non-inducer RNA was often used in excess of added protamine, and therefore there is a possibility that its action was, being a polyanion, simply to counteract the potentiating effect of protamine, a polycation, on inducer RNA.…”

Section: Cellsmentioning

confidence: 99%

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Kawade

Matsuyama

Yamamoto

et al. 1972

Japanese Journal of Microbiology

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Various single-stranded RNAs, which do not induce antiviral cell resistance in L and chick embryo cells, were found to antagonize the action of inducer RNAs such as poly(C)¥poly(I). The non-inducing RNA inhibited production of interferon stimulated by inducer RNA, but did not inhibit the action of exogenously added interferon. Two aspects were discerned in the antagonism of non-inducing RNA, namely intrinsic antagonism and anti-protamine effect. The intrinsic antagonism is the one observed in the absence of protamine. The anti-protamine effect is elimination of the potentiating action of protamine on inducing RNA [10] by non-inducing RNA in a large excess over protamine. The relative importance of the two effects will vary depending on the concentrations of protamine and non-inducing RNA used. Non-inducer RNA added to cells pretreated with inducer RNA for 1-3 hr effectively inhibited the development of antiviral cell resistance, but was not very effective when added prior to inducer RNA. RNA from MS2 phage virions was found to be an inducer in chick embryo cell but a non-inducer and antagonist in human embryo lung fibroblasts, indicating that a given RNA may possess both the inducer and the antagonist characters. The induction of interferon by viruses was not significantly inhibited by non-inducing RNA. The results obtained are consistent with an assumption that non-inducing RNA competitively inhibits the binding of inducer RNA to cellular receptor sites, although alternative interpretations are not excluded.

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Section: Cellsmentioning

confidence: 99%

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Kawade

Matsuyama

Yamamoto

et al. 1972

Japanese Journal of Microbiology

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“…He will present his most recent information about the mechanism of the establishment of the resistance. We have been engaged for several years in studies on induction of antiviral cellular resistance and interferon production in cell culture by exogenously added RNA (Kawade and Fukada, 1965;Fukada et al, 1968;Kawade and Ujihara, 1969;Matsuyama et al, 1970), stimulated by Isaacs' hypothesis (Isaacs et al, 1963) that interferon production is a cellular response to foreign nucleic acid.…”

mentioning

confidence: 99%

Symposium on Virus-Inhibiting Substance

1971

JJMSB

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Interferon-Stimulated Response Element (ISRE)-Binding Protein Complex DRAF1 Is Activated in Sindbis Virus (HR)-Infected Cells

Behr

Schieferdecker²,

Bühr³

et al. 2001

Journal of Interferon & Cytokine Research

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To elucidate the host cell defense mechanisms in response to Sindbis viral infection, we have started to characterize interferon (IFN)-stimulated response element (ISRE)-binding proteins activated in infected cells that are involved in the transcriptional induction of IFN type I-inducible genes. Using electromobility shift assays (EMSA), we detected several protein complexes with a human IFN-stimulated gene 15 (ISG15) ISRE in extracts from virus-infected L929 cells that were absent in extracts from uninfected cells. Comigration with Newcastle disease virus-activated ISRE-binding complexes, ISRE-binding specificity, supershift experiments, and conditions of formation indicate that the complexes activated by Sindbis viral infection in L929 cells correspond to DRAF1 and ISG factor 3 (ISGF3). Transfection of L929 cells with poly rI:rC induced only ISGF3. DRAF1 could be detected in Sindbis virus-infected mouse embryo fibroblasts derived from IFNR type I and type II KO mice. Viral RNA synthesis is required for activation of DRAF1.

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RNA‐Induced Interference with Animal Virus Infection

Abstract: Some RNAs, including both single-and double-stranded

Cited by 4 publications

References 7 publications

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Symposium on Virus-Inhibiting Substance

Interferon-Stimulated Response Element (ISRE)-Binding Protein Complex DRAF1 Is Activated in Sindbis Virus (HR)-Infected Cells

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