scholarly journals A novel method for the detection of early events in cell-cell fusion of Semliki Forest virus infected cells growing in monolayer cultures

1987 ◽  
Vol 95 (3-4) ◽  
pp. 283-289 ◽  
Author(s):  
C. Kempf ◽  
M. R. Michel ◽  
U. Kohler ◽  
H. Koblet
Keyword(s):  
Cell Fusion ◽  
Semliki Forest Virus ◽  
Monolayer Cultures ◽  
Infected Cells ◽  
Novel Method ◽  
Cell Cell

Semliki Forest virus induced cell-cell fusion at neutral extracellular pH

1990 ◽  
Vol 10 (4) ◽  
pp. 363-374 ◽  
Author(s):  
Christoph Kempf ◽  
Marcel R. Michel ◽  
Adames Omar ◽  
Pia Jentsch ◽  
Andreas Morell
Keyword(s):  
Cell Fusion ◽  
Semliki Forest Virus ◽  
Covalent Modification ◽  
Surface Proteins ◽  
Acidic Ph ◽  
Fusion Event ◽  
Cell Surface Proteins ◽  
Infected Cells ◽  
Peptide Segments ◽  
Cell Cell

Semliki Forest virus-induced cell-cell fusion from within was considered to exclusively occur at mildly acidic pH (<6.2). Data of this study show that such cell fusion can also be triggered by transient acidification of the cytoplasm of infected cells at an extracellular, neutral pH. Results were obtained by utilizing NH4Cl pulses combined with covalent modification of cell surface proteins. The observation implies a revision of the current consensus regarding the mechanism of Semliki Forest virus induced cell-cell fusion. We propose a model in which at least two peptide segments of the viral spike protein E1 may be involved in triggering the fusion event.

scholarly journals Virus-Mediated Cell-Cell Fusion

2020 ◽  
Vol 21 (24) ◽  
pp. 9644
Author(s):  
Héloïse Leroy ◽  
Mingyu Han ◽  
Marie Woottum ◽  
Lucie Bracq ◽  
Jérôme Bouchet ◽  
...  
Keyword(s):  
Cell Fusion ◽  
Fusion Proteins ◽  
Target Cells ◽  
Special Focus ◽  
Human Pathogens ◽  
General Process ◽  
Tissue Organization ◽  
Donor Cells ◽  
Infected Cells ◽  
Cell Cell

Cell-cell fusion between eukaryotic cells is a general process involved in many physiological and pathological conditions, including infections by bacteria, parasites, and viruses. As obligate intracellular pathogens, viruses use intracellular machineries and pathways for efficient replication in their host target cells. Interestingly, certain viruses, and, more especially, enveloped viruses belonging to different viral families and including human pathogens, can mediate cell-cell fusion between infected cells and neighboring non-infected cells. Depending of the cellular environment and tissue organization, this virus-mediated cell-cell fusion leads to the merge of membrane and cytoplasm contents and formation of multinucleated cells, also called syncytia, that can express high amount of viral antigens in tissues and organs of infected hosts. This ability of some viruses to trigger cell-cell fusion between infected cells as virus-donor cells and surrounding non-infected target cells is mainly related to virus-encoded fusion proteins, known as viral fusogens displaying high fusogenic properties, and expressed at the cell surface of the virus-donor cells. Virus-induced cell-cell fusion is then mediated by interactions of these viral fusion proteins with surface molecules or receptors involved in virus entry and expressed on neighboring non-infected cells. Thus, the goal of this review is to give an overview of the different animal virus families, with a more special focus on human pathogens, that can trigger cell-cell fusion.

scholarly journals Mechanisms of mutations inhibiting fusion and infection by Semliki Forest virus.

1996 ◽  
Vol 134 (4) ◽  
pp. 863-872 ◽  
Author(s):  
M Kielian ◽  
M R Klimjack ◽  
S Ghosh ◽  
W A Duffus
Keyword(s):  
Membrane Fusion ◽  
Cell Fusion ◽  
Semliki Forest Virus ◽  
Fusion Reaction ◽  
Infectious Clone ◽  
Low Ph ◽  
Spike Protein ◽  
Initial Reaction ◽  
Target Membrane ◽  
Cell Cell

Semliki Forest virus (SFV) infects cells by an acid-dependent membrane fusion reaction catalyzed by the virus spike protein, a complex containing E1 and E2 transmembrane subunits. E1 carries the putative virus fusion peptide, and mutations in this domain of the spike protein were previously shown to shift the pH threshold of cell-cell fusion (G91A), or block cell-cell fusion (G91D). We have used an SFV infectious clone to characterize virus particles containing these mutations. In keeping with the previous spike protein results, G91A virus showed limited secondary infection and an acid-shifted fusion threshold, while G91D virus was noninfectious and inactive in both cell-cell and virus-liposome fusion assays. During the low pH- induced SFV fusion reaction, the E1 subunit exposes new epitopes for monoclonal antibody (mAb) binding and forms an SDS-resistant homotrimer, the virus associates hydrophobically with the target membrane, and fusion of the virus and target membranes occurs. After low pH treatment, G91A spike proteins were shown to bind conformation-specific mAbs, associate with target liposome membranes, and form the E1 homotrimer. However, both G91A membrane association and homotrimer formation had an acid-shifted pH threshold and reduced efficiency compared to wt virus. In contrast, studies of the fusion-defective G91D mutant showed that the virus efficiently reacted with low pH as assayed by mAb binding and liposome association, but was essentially inactive in homotrimer formation. These results suggest that the G91D mutant is noninfectious due to a block in a late step in membrane fusion, separate from the initial reaction to low pH and interaction with the target membrane, and involving the lack of efficient formation of the E1 homotrimer.

scholarly journals Cell surface effects of human immunodeficiency virus

1988 ◽  
Vol 8 (1) ◽  
pp. 35-48 ◽  
Author(s):  
Robert F. Garry ◽  
A. Arthur Gottlieb ◽  
Kenneth P. Zuckerman ◽  
John R. Pace ◽  
Thomas W. Frank ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Cell Surface ◽  
Cell Fusion ◽  
Surface Effects ◽  
Cell Killing ◽  
Viral Envelope ◽  
Rational Approach ◽  
Immunodeficiency Virus ◽  
Infected Cells ◽  
Cell Cell

Cell killing by human immunodeficiency virus (HIV) is thought to contribute to many of the defects of the acquired immunodeficiency syndrome (AIDS). Two types of cytopathology are observed in HIV-infected cultured cells: cell-cell fusion and killing of single cells. Both killing processes appear to involve cell surface effects of HIV. A model is proposed for the HIV-mediated cell surface processes which could result in cell-cell fusion and single cell killing. The purpose of this model is to define the potential roles of individual viral envelope and cell surface molecules in cell killing processes and to identify alternative routes to the establishment of persistently-infected cells. Elucidation of HIV-induced cell surface effects may provide the basis for a rational approach to the design of antiviral agents which are selective for HIV-infected cells.

Early Events of Semliki Forest Virus-Induced Cell-Cell Fusion

Virology ◽  
1993 ◽  
Vol 196 (2) ◽  
pp. 541-547 ◽  
Author(s):  
M. Lanzrein ◽  
N. Käsermann ◽  
R. Weingart ◽  
C. Kempf
Keyword(s):  
Cell Fusion ◽  
Semliki Forest Virus ◽  
Cell Cell

Changes in membrane permeability during semliki forest virus induced cell fusion

1992 ◽  
Vol 12 (3) ◽  
pp. 221-236 ◽  
Author(s):  
Markus Lanzrein ◽  
Nicole Käsermann ◽  
Christoph Kempf
Keyword(s):  
Membrane Permeability ◽  
Cell Fusion ◽  
Semliki Forest Virus ◽  
Divalent Cations ◽  
Ph Dependence ◽  
Syncytium Formation ◽  
Permeability Change ◽  
Infected Cells ◽  
Ph Dependent ◽  
Radiolabeled Compounds

The infection of Aedes albopictus cells by Semliki Forest virus (SFV) is a non lytic event. Exposure of infected cells to mildly acidic pH (<6.2) leads to syncytium formation. This polykaryon formation is accompanied by an influex of protons into the cells (Kempf et al. Biosci. Rep. 7, 761–769, 1987). We have further investigated this permeability change using various fluorescent or radiolabeled compounds. A significant, pH dependent increase of the membrane permeability to low molecular weight compounds (Mr<1000) was observed when infected cells were exposed to a pH<6.2. The pH dependence of the peremability change was very similar to the pH dependence of cell-cell fusion. The permeability change was sensitive to divalent cations, protons and anionic antiviral drugs such as trypan blue. The nature of this virus induced, pH dependent permeability change is discussed.

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