An Ultrastructural Study of Interspecific Cell Fusion Induced by Inactivated Sendai Virus

1966 ◽  
Vol 1 (4) ◽  
pp. 401-406
Author(s):  
E. E. SCHNEEBERGER ◽  
H. HARRIS
Keyword(s):  
Cell Fusion ◽  
Hela Cells ◽  
Sendai Virus ◽  
Electron Microscopic Examination ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Large Numbers ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Cells ◽  
Cytoplasmic Bridges

An electron-microscopic examination was made of the process of cell fusion induced by Sendai virus inactivated by ultraviolet light. Ehrlich ascites cells, HeLa cells, rabbit macrophages, rat lymphocytes and nucleated hen erythrocytes were chosen for study because it had previously been shown that these cells could be fused together, with varying degrees of facility, to form artificial heterokaryons. Cells which had large numbers of microvilli on their surfaces fused together more readily than those which had not, but the presence of microvilli was not essential for fusion to occur. Fusion appeared in all cases to be initiated by the formation of small cytoplasmic bridges between the cells; but virus particles, although present elsewhere on the surface of the cells, were not detected at or near the cytoplasmic bridges. HeLa-hen erythrocyte heterokaryons were formed by the fusion of HeLa cells with red cell ghosts.

Electron Microscopic Observations on the Rescue of SV40 Virus From Transformed Cells

1972 ◽  
Vol 30 ◽  
pp. 278-279
Author(s):  
Ronald Glaser ◽  
Ross Farrugia
Keyword(s):  
Electron Microscopy ◽  
Cell Fusion ◽  
Sendai Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Transformed Cells ◽  
Density Gradients ◽  
Electron Microscopic ◽  
Sv40 Virus ◽  
Virus Particles

Several laboratories have reported that simian virus 40 (SV40) was rescued from transformed cells when the nonproducing cells were cocultivated or fused in the presence of ultraviolet inactivated Sendai virus (UV-SV), to potentially susceptible cells. Evidence obtained from studies in which nuclei from heterokaryons were isolated and separated on density gradients, indicated that rescued virus was first detected in the transformed nuclei of the heterokaryons formed during cell fusion. The present study was performed to determine how long after fusion SV40 virus particles could be found in the nuclei of the heterokaryons and to investigate the site of rescue by electron microscopy.

Cell-fusion properties of Sendai virus prepared by polyethylene-glycol precipitation

1972 ◽  
Vol 18 (5) ◽  
pp. 607-610 ◽  
Author(s):  
Gregory J. Cook ◽  
Lorne A. Babiuk ◽  
James B. Hudson
Keyword(s):  
Cell Fusion ◽  
Sendai Virus ◽  
Allantoic Fluid ◽  
Electron Microscopic Examination ◽  
Electron Microscopic ◽  
Polyethylene Glycol Precipitation ◽  
Chicken Eggs ◽  
Fusion Ability ◽  
Maximum Retention ◽  
Embryonated Chicken

Sendai virus was concentrated from the allantoic fluid of embryonated chicken eggs by polyethyleneglycol (PEG) precipitation. A concentration of 6–8% PEG sufficed to precipitate essentially all of the virus (measured by hemagglutination) with maximum retention of cell-fusion ability. Electron-microscopic examination of the 6% PEG pellet revealed only intact virions. Thus the method is suitable for preparing Sendai virus for cell-fusion experiments.

scholarly journals Studies of membrane fusion. IV. Fusion of HeLa cells with Sendai virus

1979 ◽  
Vol 36 (1) ◽  
pp. 73-84
Author(s):  
S. Knutton
Keyword(s):  
Plasma Membrane ◽  
Membrane Fusion ◽  
Cell Fusion ◽  
Hela Cells ◽  
Sendai Virus ◽  
Freeze Fracture ◽  
Viral Envelope ◽  
Cell Plasma Membrane ◽  
Virus Particles ◽  
Cell Plasma

The Sendai virus-induced fusion of HeLa cells has been studied by freeze-fracture electron microscopy. Freeze-fracture observations confirm previous scanning electron-microscope studies (1977) and show that at 4 degrees C virus particles bind to the cell surface and that cell agglutination results from the crosslinking by virus particles of microvilli on adjacent cells. Incubation at 37 degrees C initiates a change in viral envelope structure and fusion of ‘altered’ virus particles with the cell plasma membrane. Fusion of a virus particle with two crosslinked cells is probably the membrane fusion event which initiates cell-cell fusion; fusion is completed as a result of virally induced cell swelling. Lateral diffusion of viral envelope components following virus-cell fusion and, in some instances, an aggregation of plasma membrane intramembrane particles occurs in swollen cells. These observations show that the mechanisms of viral envelope-cell and probably cell-cell fusion are the same as have been reported for erythrocytes. Although endocytosis of intact virus particles does occur, the specialized cell-mediated mechanism for fusion of the viral envelope with the cell plasma membrane suggests that this, and not viropexis, is the mechanism of Sendai virus infection.

Viruses Associated with Lymphocystis Disease and Dermal Sarcoma of Walleye (Stizostedion vitreum vitreum)

1976 ◽  
Vol 33 (11) ◽  
pp. 2408-2419 ◽  
Author(s):  
Tats Yamamoto ◽  
Richard D. Macdonald ◽  
Douglas C. Gillespie ◽  
Russell K. Kelly
Keyword(s):  
Electron Microscopic Examination ◽  
The Body ◽  
Stizostedion Vitreum ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Large Numbers ◽  
Lymphocystis Disease ◽  
Spawning Run ◽  
Tumor Types ◽  
Dermal Sarcoma

Gross examination of a spawning run of walleye (Stizostedion vitreum vitreum) showed a large proportion of fish to have tumors on the body and fins that appeared to be characteristic of lymphocystis disease. Light and electron microscopic examination revealed the presence of two distinct tumor types. One was characteristic of lymphocystis, consisting of typical enlarged nonneoplastic cells surrounded by hyaline layers and containing many 260 nm diameter lymphocystis virus particles in the cytoplasm. The other tumor, referred to as a dermal sarcoma, consisted of a solid mass of normal-sized cells and contained in the cytoplasm large numbers of 135 nm diameter virus particles referred to as walleye dermal sarcoma (WDS) virus. The WDS virus was similar in appearance to the leukoviruses and, with its outer layer sectioned tangentially, exhibited symmetry like a member of a leukovirus group designated by Fenner as subgenus C.

Studies of membrane fusion. I. Paramyxovirus-induced cell fusion, a scanning electron-microscope study

1977 ◽  
Vol 28 (1) ◽  
pp. 179-188
Author(s):  
S. Knutton ◽  
D. Jackson ◽  
M. Ford
Keyword(s):  
Cell Surface ◽  
Cell Fusion ◽  
Hela Cells ◽  
Cell Swelling ◽  
Cell Contact ◽  
Cell Agglutination ◽  
Scanning Electron Microscope Study ◽  
Virus Particles ◽  
Scanning Electron ◽  
Cell Cell

Fusion of erythrocytes and HeLa cells with Sendai and Newcastle disease viruses has been studied by scanning electron microscopy. Most virus particles are spherical but vary in diameter from approximately 200 to approximately 600 nm. At 4 degrees C virus particles bind randomly to the cell surface and at high cell densities cross-linking of adjacent cells by virus particles results in cell agglutination. Cell-cell fusion takes place when the agglutinated cell suspension is warmed to 37 degrees C. Fusion is initiated at sites of cell-cell contact and is accompanied in all cases by cell swelling. In the case of suspension HeLa cells, virally mediated cell swelling involves an ‘unfolding’ of cell surface microvilli and results in the formation of smooth-surfaced single or fused cells. With erythrocytes, swelling results in haemolysis. There is a dramatic reduction in the numbers of virus particles bound to cells following fusion.

Studies of membrane fusion. V. Fusion of erythrocytes with non-haemolytic Sendai virus

1979 ◽  
Vol 36 (1) ◽  
pp. 85-96
Author(s):  
S. Knutton
Keyword(s):  
Membrane Fusion ◽  
Cell Fusion ◽  
Erythrocyte Membrane ◽  
Sendai Virus ◽  
Lateral Diffusion ◽  
Viral Envelope ◽  
Cell Swelling ◽  
Viral Membrane ◽  
Cytoplasmic Bridges ◽  
Viral Envelopes

The fusion of human erythrocytes with non-haemolytic ‘1-day’ Sendai virus has been studied by electron microscopy. The mechanism of viral envelope-cell fusion is the same as that described previously for haemolytic ‘3-day’ Sendai virus except that fusion is frequently arrested at an initial stage when 2 segments of smooth linear viral membrane fuse and become incorporated into the erythrocyte membrane. After longer periods of incubation at 37 degrees C, in addition to many partly fused virus particles, long (up to 4 micrometer) lengths of smooth linear viral membrane are seen within the erythrocyte membrane which arise by linear aggregation of shorter (approximately 0.25 micrometer long) segments of smooth linear membrane derived from individual fused viral envelopes. Cell-Cell fusion, as a result of the fusion of a viral envelope with 2 adjacent erythrocytes also occurs but, in the absence of cell swelling, fusion is arrested at this stage with cells joined by one (or more) small cytoplasmic bridges. Typical fused cells are produced if such cells are swollen with hypotonic buffer. These observations provide further evidence that membrane fusion and cell swelling are distinct events in cell fusion and that cell swelling is the driving force both for completing the incorporation of the viral envelope into the cell membrane and for expanding cells connected by small cytoplasmic bridges to form spherical fused cells. Little lateral diffusion of viral envelope components occurs in the absence of cell swelling; in fact, some aggregation of components occurs. Comparison with previous studies using haemolytic ‘3-day’ Sendai virus suggests that virally induced cell swelling perturbs membrane structure so as to allow the rapid lateral diffusion of integrated viral envelope components.

The Analysis of Malignancy by Cell Fusion

1971 ◽  
Vol 8 (3) ◽  
pp. 673-680
Author(s):  
U. BREGULA ◽  
G. KLEIN ◽  
H. HARRIS
Keyword(s):  
Cell Fusion ◽  
Chromosomal Analysis ◽  
Cell Populations ◽  
Hybrid Cells ◽  
Parental Chromosome ◽  
Chromosomal Constitution ◽  
Diploid Fibroblasts ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Cells

When Ehrlich ascites cells were fused with diploid fibroblasts, isolated directly from the animal, the resulting hybrid cells regularly produced progressive tumours. However, an analysis of a range of clonal populations of these hybrid cells, each derived from a separate primary fusion, revealed that the chromosomal constitution of these cells was highly unstable; all cell populations were found to have already undergone substantial chromosome losses by the time enough cells were available to permit chromosomal analysis. Thus, although these hybrid cells were highly tumorigenic, the tumours arising from them were not composed of cells with complete parental chromosome sets, but of cells from which some chromosomes had been eliminated.

scholarly journals Role of Helicobacter felis in Chronic Canine Gastritis

1992 ◽  
Vol 29 (6) ◽  
pp. 487-494 ◽  
Author(s):  
A. Lee ◽  
S. Krakowka ◽  
J. G. Fox ◽  
G. Otto ◽  
K. A. Eaton ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Plasma Cells ◽  
Serum Antibody ◽  
Electron Microscopic Examination ◽  
Gastric Mucus ◽  
Electron Microscopic ◽  
Helicobacter Felis ◽  
Large Numbers ◽  
Histopathologic Changes ◽  
Gastric Parietal Cells

Five gnotobiotic Beagle dogs were orally inoculated with a pure culture of Helicobacter felis. The remaining two littermates served as contact controls. Thirty days after infection, all animals were euthanatized and specimens were collected for evaluation. In infected dogs, H. felis was recovered from all areas of the stomach. Colonization was heaviest in the fundus and antrum. H. felis was not cultured from any segment of the gastrointestinal tract distal to the duodenum. Two weeks after infection, all five infected dogs had detectable IgM and IgG serum antibody to H. felis, whereas control dogs had no measurable H. felis serum antibody throughout the study. Histopathologic changes in the stomachs of infected dogs included large numbers of lymphoid nodules throughout all regions of the gastric mucosa and were most numerous in the fundus and body. A mild, diffuse lymphocytic infiltrate with small numbers of plasma cells and eosinophils was also present in the subglandular region of all portions of the gastric mucosa. Electron microscopic examination revealed large numbers of spiral-shaped H. felis in gastric mucus adjacent to or superimposed over the areas of inflammation. Occasionally, however, H. felis was observed within the canaliculi of gastric parietal cells. Histopathologic changes in the stomachs of the contact control dogs were limited to focal infiltrates of eosinophils and small aggregates of lymphocytes in the subglandular portions of the gastric mucosa in one animal. Infection with H. felis is a likely cause of naturally occurring lymphofollicular gastritis.

Watermelon mosaic virus 1 and 2 in Queensland cucurbit crops

1978 ◽  
Vol 29 (6) ◽  
pp. 1235 ◽  
Author(s):  
RS Greber
Keyword(s):  
Mosaic Virus ◽  
Virus Type ◽  
Electron Microscopic Examination ◽  
Watermelon Mosaic Virus ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Cellular Inclusions ◽  
Differential Hosts

Watermelon mosaic virus type 1 (WMV-1) has not previously been reported from Australia and has become prevalent in Queensland only since 1970. Watermelon mosaic virus type 2 (WMV-2) continues to reach a high incidence in marrow (Cucurbita pepo) and pumpkin (Cucurbita maxima and Cucurbita moschata) crops, WMV-2 is rarely isolated from watermelons (Citrullus vulgaris) in which epidemics of WMV-1 now cause serious reductions in yield. The Queensland Blue cultivar of C. maxima, the most important cucurbit crop, produces severely distorted fruit following infection by WMV-1, although it is little affected by WMV-2. Physical properties of these WMV isolates and electron microscopic examination of the virus particles and associated cellular inclusions showed them to be similar to those reported elsewhere, but there were some distinctive host reactions for the WMV-2 isolates. No resistance to either WMV-1 or WMV-2 was found in commercially available C. pepo, C. maxima or C. vulgaris. The resistance of Cucumis metuliferus to Australian WMV-1 isolates was confirmed, and a source of resistance to both WMV-1 and WMV-2 was found in Lagenaria siceravia. Methods of separation of WMV-1 and WMV-2 from mixed isolates and methods for the identification of each on differential hosts and by serology were shown to be effective.

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