Na and K Changes in Animal Virus-infected HeLa Cells

Nair, C. N.

doi:10.1099/0022-1317-65-6-1135

Cited by 11 publications

(11 citation statements)

References 12 publications

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“…The alterations in ion concentration occurring in the cytoplasm of virus-infected cells could favor virus replication, by enhancing the intracellular concentration of sodium ions. This might promote translation of viral versus cellular mRNAs, because translation of mRNAs from many cytolytic animal viruses, including reoviruses, is fairly resistant to high sodium concentrations, whereas high sodium concentrations are inhibitory for the translation of most cellular mRNAs (52)(53)(54)(55)(56)(57). On the other hand, progressive membrane damage is thought to promote cell lysis and virus release, facilitating virus spreading to surrounding cells (9,36).…”

Section: Membrane Permeabilization By Avian Reovirus Requires Viral Pmentioning

confidence: 99%

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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Section: Membrane Permeabilization By Avian Reovirus Requires Viral Pmentioning

confidence: 99%

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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“…In other systems, changes in intracellular Na + and K ÷ levels are detected after viral inhibition of cellular protein synthesis. Therefore, they do not seem to be a primary cause of the observed inhibition (Hackstadt & Mallavia, 1982;Lacal & Carrasco, 1982;Mizzen et al, 1987;Francoeur & Stanners, 1978;Nair, 1984).…”

Section: Introductionmentioning

confidence: 99%

Rotavirus infection alters Na+ and K+ homeostasis in MA-104 cells

Castillo

Ludert²,

Sánchez³

et al. 1991

Journal of General Virology

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Infection of MA-104 cells with the OSU strain of rotavirus induced an increase in Na ÷ and a decrease in K ÷ intracellular concentrations, starting at 4 h postinfection. These changes were not related to an inhibition of the Na+/K ÷ pump since ouabain-sensitive S6Rb uptake was augmented in rotavirus-infected cells compared to control cells, whereas the [3H]ouabain binding and Na÷/K + ATPase activity in the cell homogenate were unaffected. Furosemide-sensitive S6Rb uptake (Na+/K÷/2CI -cotransport) was not modified by the infection. Passive S6Rb efflux and ZZNa influx were augmented in infected cells suggesting an increase in the plasma membrane permeability. The increase in intracellular Na ÷ concentration might be responsible for the observed stimulation of the Na+/K + pump. This effect was dependent upon the synthesis of viral proteins because it was abolished by addition of cycloheximide up to 4 h post-infection. Prevention of the increase in intracellular Na ÷ by the use of low Na ÷-containing media did not modify the pattern of protein synthesis. This suggests that changes in intracellular Na + and K ÷ concentrations were not related to shutoff of cellular protein synthesis. Alterations of ion contents in the rotavirus-infected enterocytes might impair intestinal absorptive capacity before the appearance of histopathological lesions.

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“…On the other hand many investigators have found that although a virus may induce changes in membrane permeability and an accompanying change in the levels of Na + and K +, this does not correlate with the inhibition of protein synthesis in infected cells (VSV, Francoeur & Stanners, 1978;poliovirus, Nair, 1981; encephalomyocarditis virus and human rhinovirus, Nair, 1984;Sindbis virus, Ulug & Bose, 1985). Nair (1984) monitored the Na + and K + changes and cytotoxic effects in HeLa cells infected with encephalomyocarditis virus, human rhinovirus or VSV.…”

Section: Discussionmentioning

confidence: 99%

“…Nair (1984) monitored the Na + and K + changes and cytotoxic effects in HeLa cells infected with encephalomyocarditis virus, human rhinovirus or VSV. In all three cases it was found that changes in Na + and K + levels followed viral inhibition of cellular protein synthesis, and therefore do not trigger shut-off of host cell protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

“…The alteration of intracellular monovalent cation levels (particularly Na + and K +) has been observed in lytic infections by several animal viruses (Carrasco & Smith, 1976;Hackstadt & Mallavia, 1982;Nair, 1984;Ulug et al, 1984) and is presumed to contribute to the cytopathic effects seen in the infected cells. It has been proposed that changes in plasma membrane permeability account for the altered intracellular cation levels (Carrasco, 1977).…”

Section: Introductionmentioning

confidence: 99%

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Translational Regulation in Mouse Hepatitis Virus Infection Is Not Mediated by Altered Intracellular Ion Concentrations

Mizzen¹,

Macintyre

Wong

et al. 1987

Journal of General Virology

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SUMMARYInfection of mouse L-2 fibroblasts with mouse hepatitis virus (MHV) results in strong inhibition of host cell protein synthesis. Since it has been suggested in other virus systems that translational control is modulated by changes in the intracellular ionic environment, we investigated the possible occurrence of similar changes during MHV infection. Membrane permeability to extracellular sodium ions was measured by culturing MHV-infected cells in the presence of 22Na+. Sodium influx into MHVinfected cells rose dramatically from 4 to 6 h post-infection. This influx correlated chronologically with the expression of MHV-mediated cell fusion. Cell fusion was blocked by the addition of a monoclonal antibody against the MHV E 2 glycoprotein. This addition also resulted in a reduction in the normal influx of 22Na+, suggesting that E 2 expression was responsible, directly or indirectly, for the increased permeability to sodium ions in infected cells. Cultures of MHV-infected cells were labelled with [35S]methionine in the presence of medium supplemented with sodium chloride at final concentrations ranging from 150 mM to 350 mM. Incorporation of radiolabel into proteins decreased with increasing NaC1 concentration; however, the ratio of viral to cellular protein synthesis remained relatively constant. Similarly, alteration of intracellular Na + and K + levels by treatment of infected cells with ouabain had little effect on the pattern of viral/cellular protein synthesis. Using monoclonal anti-E_, antibody to inhibit Na + influx, we demonstrated normal inhibition of host cell protein synthesis. We therefore conclude that MHV-induced shut-offof host translation is not mediated by changes in intracellular Na + concentrations.

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Na and K Changes in Animal Virus-infected HeLa Cells

Cited by 11 publications

References 12 publications

Modification of Late Membrane Permeability in Avian Reovirus-infected Cells

Modification of Late Membrane Permeability in Avian Reovirus-infected Cells

Rotavirus infection alters Na+ and K+ homeostasis in MA-104 cells

Translational Regulation in Mouse Hepatitis Virus Infection Is Not Mediated by Altered Intracellular Ion Concentrations

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