Inhibition of animal virus production by means of translation inhibitors unable to penetrate normal cells

Benedetto, A.; Rossi, Giovanni Battista; Amici, Carla; Belardelli, Filippo; Cioé, Livia; Carruba, Giuseppe; Carrasco, Luís

doi:10.1016/0042-6822(80)90227-5

Cited by 45 publications

(32 citation statements)

References 14 publications

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“…Whatever the reason for the rounding-up and other cytopathic changes seen in VSV infections (Bablanian, 1975), entry of water or alteration of Na+/K + content does not appear to be one of them. Nor do these results support the hypothesis that sensitivity of the protein-synthesizing system to hygromycin B in VSV-infected cells is due to membrane leakiness (Benedetto et al, 1980). Furthermore, it is clear that, in contrast to the hypothesis of Carrasco (1977), neither virus synthesis, which had reached a maximum by 4 h post-infection (Fig.…”

Section: Vsv-infected Cellscontrasting

confidence: 54%

Effect of Vesicular Stomatitis Virus and Semliki Forest Virus on Uptake of Nutrients and Intracellular Cation Concentration

Gray

Micklem

Brown

et al. 1983

Journal of General Virology

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Section: Vsv-infected Cellscontrasting

confidence: 54%

Effect of Vesicular Stomatitis Virus and Semliki Forest Virus on Uptake of Nutrients and Intracellular Cation Concentration

Gray

Micklem

Brown

et al. 1983

Journal of General Virology

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“…We found that the plasma membrane of S1133-infected CEF becomes permeabilized at late, but not early, infection times, and that the perturbed membrane allows increased influx and efflux of metabolites. Enhanced membrane permeability at late infection times has been also observed in cells infected with flaviviruses (28), herpesviruses, rhabdoviruses (29), paramyxoviruses (29), papovaviruses (30), picornaviruses (31), retroviruses (32,33), and togaviruses (34).…”

Section: Membrane Permeabilization By Avian Reovirus Requires Viral Pmentioning

confidence: 97%

Modification of Late Membrane Permeability in Avian Reovirus-infected Cells

Bodelón

Labrada²,

Martı́nez-Costas

et al. 2002

Journal of Biological Chemistry

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Infection of chicken embryo fibroblasts by avian reovirus induces an increase in the permeability of the host plasma membrane at late, but not early, infection times. The absence of permeability changes at early infection times, as well as the dependence of late membrane modification on both viral protein synthesis and an active exocytic route, suggest that a virus-encoded membrane protein is required for avian reovirus to permeabilize cells. Further studies revealed that expression of nonstructural p10 protein in bacterial cells arrested cell growth and enhanced membrane permeability. Membrane leakiness was also observed following transient expression of p10 in BSC-40 monkey cells. Both its permeabilizing effect and the fact that p10 shares several structural and physical characteristics with other membrane-active viral proteins indicate that p10 is an avian reovirus viroporin. Furthermore, the fusogenic extracellular NH 2 -terminal domain of p10 appears to be dispensable for permeabilizing activity, because its deletion entirely abolished the fusogenic activity of p10, without affecting its ability to associate with cell membranes and to enhance membrane permeability. Similar properties have reported previously for immunodeficiency virus type I transmembrane glycoprotein gp41. Thus, like gp41, p10 appears to be a multifunctional protein that plays key roles in virus-host interaction.Cytolytic viruses induce profound injurious effects in susceptible host cells, resulting in morphological, structural, and biochemical changes and in cell degeneration. A widespread phenomenon during viral infection is the alteration of the permeability of the host plasma membrane (reviewed in Refs.

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“…After 18 h at 37 °C, supernatants were collected and titrated on L929 cells (Belardelli et al, 1984). In some experiments, VSV yields were titrated by plaque assay, as described in detail elsewhere (Benedetto et al, 1980). For HSV-1, after a 2 h incubation at 37 °C, cells were washed and incubated for 48 h in 1 ml of nutrient medium.…”

Section: Methodsmentioning

confidence: 99%

Cyclic AMP-mediated inhibition of vesicular stomatitis virus and herpes simplex virus replication in mouse macrophage-like cells

Borghi

Marzio

Varano

et al. 1992

Journal of General Virology

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In this study, we have analysed the effects of cAMP inducers on the multiplication of vesicular stomatis virus (VSV) and herpes simplex virus type 1 (HSV-1) in mouse macrophage-like cells. The addition ofdibutyryl cAMP (dB-cAMP) or cholera toxin to resting peritoneal macrophages aged in vitro or P388D1 cells resulted in a 10-to 100-fold reduction of VSV yield compared to control cultures. In contrast, no cAMP-dependent inhibition was found in VSV-infected L929 cells. In macrophage-like cells, the dB-cAMP-induced antiviral state was not inhibited by antibodies to interferon (IFN)-~//] and did not correlate with any increase in the intracellular levels of 2-5 oligo(A) synthetase. Dibutyryl cAMP did not inhibit virus yields in mouse macrophages infected with encephalomyocarditis virus. In P388D~ cells, the addition of dB-cAMP resulted in an approximately 10-fold inhibition of HSV-1 replication with respect to control cultures, as evaluated both by TCIDso and plaque assays on Vero cells. Dibutyryl cAMP did not affect VSV binding or entry into mouse macrophages and the cAMPmediated anti-VSV state was significantly reduced by inhibitors of protein kinase C (i.e. staurosporine and H7). These data suggest that macrophages may acquire resistance to infection by VSV and HSV-1 after treatment with cAMP inducers. This cAMP-mediated antiviral activity does not depend on the modulation of the endogenous IFN system, suggesting that macrophages exhibit multiple resistance mechanisms (i.e. IFN-dependent and IFN-independent) to maintain their intrinsic antiviral activity.

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Inhibition of animal virus production by means of translation inhibitors unable to penetrate normal cells

Cited by 45 publications

References 14 publications

Effect of Vesicular Stomatitis Virus and Semliki Forest Virus on Uptake of Nutrients and Intracellular Cation Concentration

Effect of Vesicular Stomatitis Virus and Semliki Forest Virus on Uptake of Nutrients and Intracellular Cation Concentration

Modification of Late Membrane Permeability in Avian Reovirus-infected Cells

Cyclic AMP-mediated inhibition of vesicular stomatitis virus and herpes simplex virus replication in mouse macrophage-like cells

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