The effect of Ca2+ on virus-cell fusion and permeability changes

Micklem, K. J.; Nyaruwe, A; Alder, G. M.; Pasternak, C. A.

doi:10.1016/0143-4160(84)90030-7

Cited by 18 publications

(5 citation statements)

References 33 publications

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“…A similar result is obtained if virus-cell fusion is measured by a fluorescence enhancement technique (Wyke et al 1980;Micklem et al 1984). The fact that Ca 2 + prevents the permeability change induced by late harvest Sendai virus without affecting its ability to fuse, and hence prevents syncitium formation (Knutton and Pasternak 1979), is incidentally another good argument for dissociating fusion (i. e. stage 2) from reshaping mechanisms (i.e.…”

Section: The Role Of Calcium In Membrane Fusionsupporting

confidence: 57%

Mechanisms of Membrane Fusion

Pasternak

1990

Biomechanics of Active Movement and Deformation of Cells

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Section: The Role Of Calcium In Membrane Fusionsupporting

confidence: 57%

Mechanisms of Membrane Fusion

Pasternak

1990

Biomechanics of Active Movement and Deformation of Cells

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“…The successful delivery of high molecular weight viral genomic material can occur even when fusing membranes are moderately leaky. The propensity of viral fusogenic proteins (e.g., of influenza, Semiliki-Forest, or Sendai virus) to induce leakage of content of fusing compartments, erythrocyte hemolysis in particular, has been repeatedly reported (Impraim et al, 1980;Micklem et al, 1984;Wharton et al, 1986;Niles et al, 1990;Samsonov et al, 2002). Is this leakage involved in actual rearrangements of membranes during fusion?…”

Section: Discussionmentioning

confidence: 99%

Membrane Permeability Changes at Early Stages of Influenza Hemagglutinin-Mediated Fusion

Frolov

Dunina-Barkovskaya

Samsonov

et al. 2003

Biophysical Journal

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While biological membrane fusion is classically defined as the leak-free merger of membranes and contents, leakage is a finding in both experimental and theoretical studies. The fusion stages, if any, that allow membrane permeation are uncharted. In this study we monitored membrane ionic permeability at early stages of fusion mediated by the fusogenic protein influenza hemagglutinin (HA). HAb2 cells, expressing HA on their plasma membrane, fused with human red blood cells, cultured liver cells PLC/PRF/5, or planar phospholipid bilayer membranes. With a probability that depended upon the target membrane, an increase of the electrical conductance of the fusing membranes (leakage) by up to several nS was generally detected. This leakage was recorded at the initial stages of fusion, when fusion pores formed. This leakage usually accompanied the "flickering" stage of the early fusion pore development. As the pore widened, the leakage reduced; concomitantly, the lipid exchange between the fusing membranes accelerated. We conclude that during fusion pore formation, HA locally and temporarily increases the permeability of fusing membranes. Subsequent rearrangement in the fusion complex leads to the resealing of the leaky membranes and enlargement of the pore.

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“…The haemolytic action of paramyxoviruses like Sendai or Newcastle Disease virus has long been known to be prevented by high concentrations of Ca 2+ [24]. Since then the action of Ca 2+ has been shown to be on the lesion itself and not limited to the lysis of red cells [25] or to the action of haemolytic viruses [26]; indeed red cells are relatively insensitive to protection by Ca 2+, compared with other cells [27,28]. Zn 2+ inhibits haemolysis induced by a number of agents [29], including activated complement [30], and again this finding has been extended to non-erythroid cells [1,31]; trivalent ions are also active [32][33][34], but their toxicity in other regards, as well as the fact that they tend to bind irreversibly to the cells they are protecting, has led Ca 2÷ and Zn 2+ to emerge as the ions most likely to be of physiological importance [35], with Zn 2+ the only ion likely to be of clinical benefit (e.g.…”

Section: Trivalent and Divalent Cationsmentioning

confidence: 99%

Membrane damage: common mechanisms of induction and prevention

Pasternak¹

1992

FEMS Microbiology Letters

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SUMMARYCommon features in the induction of pores by various agents are as follows: induction is stochastic and progressive; damage by different agents is often synergistic and limited. The prevention of membrane damage is affected by trivalent and divalent cations, by low pH, by low ionic strength and by high osmotic pressure. The inhibitory role of protons and divalent cations is considered in greater detail: pore-forming agents can be classified into two groups: channels across planar lipid bilayers induced by the first group display voltage-sensitive, reversible inhibition by divalent cations; channels of the second group show voltage-insensitive, irreversible inhibition by divalent cations. A search for the ligands to which divalent cations and protons bind has proved elusive. Comparison with the phenomenon of

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The effect of Ca2+ on virus-cell fusion and permeability changes

Cited by 18 publications

References 33 publications

Mechanisms of Membrane Fusion

Mechanisms of Membrane Fusion

Membrane Permeability Changes at Early Stages of Influenza Hemagglutinin-Mediated Fusion

Membrane damage: common mechanisms of induction and prevention

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