Inhibition of Phosphatidylethanolamine Biosynthesis in Baby Hamster Kidney-21 Cells Infected with Semliki Forest Virus

1975 ◽  
Vol 53 (9) ◽  
pp. 950-957 ◽  
Author(s):  
Dennis E. Vance ◽  
Rita M. Dahlke
Keyword(s):  
Viral Infection ◽  
Nadh Dehydrogenase ◽  
Semliki Forest Virus ◽  
Kidney Cells ◽  
Baby Hamster Kidney ◽  
Microsomal Enzymes ◽  
Similar Reduction ◽  
Intact Cells ◽  
Infected Cells ◽  
Baby Hamster Kidney Cells

Semliki Forest virus inhibits phosphatidylethanolamine biosynthesis in baby hamster kidney-21 cells 6 h after infection. Viral infection reduced the incorporation of [1,2-14C]-ethanolamine into intact cells by approximately 50%. A similar reduction in the activity of the ethanolaminephosphotransferase (EC 2.7.8.1) was also observed. The apparent Km for CDPethanolamine was 60 μM for the microsomal enzymes from infected or mock-infected cells. In addition, exogenous diglyceride only stimulated by 1.5-fold the ethanolaminephosphotransferase from virus- or mock-infected cells, whereas the same diglyceride preparations stimulated the cholinephosphotransferase (EC 2.7.8.2) from baby hamster kidney cells by sixfold. Generation of endogenous diglyceride by pretreatment of the microsomes with phospholipase C (EC 3.1.4.3) stimulated the activity of the cholinephosphotransferase but not the ethanolaminephosphotransferase. Semliki Forest virus does not inhibit all microsomal enzymes, since the activities of NADH- K3Fe(CN)6 reductase and NADH dehydrogenase (EC 1.6.99.3) were not affected. The ethanolaminephosphotransferase from virus- and mock-infected cells showed similar profiles of activity as a function of temperature; this result and other studies suggest that that membranous environment of the ethanolaminephosphotransferase was not significantly modified by the virus.

scholarly journals Immunocytochemical study of the partition and distribution of Sindbis virus glycoproteins in freeze-fractured membranes of infected baby hamster kidney cells.

1985 ◽  
Vol 101 (4) ◽  
pp. 1300-1306 ◽  
Author(s):  
M R Torrisi ◽  
S Bonatti
Keyword(s):  
Plasma Membrane ◽  
Sindbis Virus ◽  
Plasma Membranes ◽  
Protein A ◽  
Kidney Cells ◽  
Baby Hamster Kidney ◽  
Immunocytochemical Study ◽  
Viral Glycoproteins ◽  
Infected Cells ◽  
Baby Hamster Kidney Cells

Sindbis virus-infected baby hamster kidney cells were analyzed by thin section fracture-label. Specific immunolabel with antiviral glycoprotein antibodies or with conventional lectin label (wheat germ agglutinin) were used in conjunction with colloidal gold-conjugated protein A or ovomucoid, respectively. In addition, intact infected cells were analyzed with both labeling procedures. Experiments with Sindbis infected-chick embryo fibroblast cells were carried out as controls. Viral transmembrane glycoproteins appeared present in freeze-fractured inner and outer nuclear membrane, endoplasmic reticulum, Golgi stacks and vesicles, and plasma membranes; a clear preferential partition with the exoplasmic faces of all intracellular membranes was observed. By contrast, at the plasma membrane level, Sindbis glycoproteins were found to partition preferentially with the protoplasmic face. It seems likely that this protoplasmic partition is related to the binding with the nucleocapsid that takes place during the budding of the virus. At the cell surface, viral glycoproteins always appeared clustered and were predominantly associated with budding figures: moreover, large portions of the plasma membrane were devoid of both glycoproteins and budding viruses.

scholarly journals Polyphosphoinositide metabolism in baby-hamster kidney cells infected with herpes simplex virus type 1

1986 ◽  
Vol 237 (3) ◽  
pp. 707-712 ◽  
Author(s):  
N Langeland ◽  
L Haarr ◽  
H Holmsen
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Simplex Virus Type ◽  
Kidney Cells ◽  
Baby Hamster Kidney ◽  
Infected Cells ◽  
Simplex Virus ◽  
Baby Hamster Kidney Cells ◽  
Polyphosphoinositide Metabolism

The incorporation of [32P]Pi and [3H]inositol into the inositol lipids of baby-hamster kidney cells was studied in herpes-simplex-virus-type-1(HSV-1)-infected and mock-infected cells. The infection was conducted during incorporation of, as well as after prelabelling with, the precursors. These methods were used in order to study both synthesis de novo of, and steady-state changes in, the phosphoinositides. Both with infection during labelling, and after prelabelling, we found increased [32P]- and [3H]-phosphatidylinositol 4,5-bisphosphate (PIP2) and decreased [32P]- and [3H]-phosphatidylinositol 4-monophosphate in infected as compared with mock-infected cells, whereas no effect was observed on phosphatidylinositol. This altered inositol-lipid metabolism was (at least in the case of PIP2) not present until 3-6 h after infection and remained stable, or increased slightly, throughout the infection period. Polyphosphoinositide metabolism constitutes an important step in signal processing in many forms of cellular stimulation, and the results obtained suggest that HSV-1 infection may induce such events in our cell system.

scholarly journals Effect of virus infection on the stability and synthesis of actinomycin-resistant ribonucleic acid in baby-hamster kidney cells

1967 ◽  
Vol 105 (3) ◽  
pp. 987-993 ◽  
Author(s):  
S J Martin ◽  
F. Brown
Keyword(s):  
Base Composition ◽  
Rna Synthesis ◽  
Sucrose Gradient ◽  
Foot And Mouth Disease ◽  
Kidney Cells ◽  
Baby Hamster Kidney ◽  
Mouth Disease Virus ◽  
Infected Cells ◽  
The Stability ◽  
Baby Hamster Kidney Cells

1. The sucrose-gradient pattern of 32P-labelled RNA synthesized in actinomycintreated baby-hamster kidney cells infected with foot-and-mouth-disease virus depends greatly on the period of labelling. 2. Fractions are formed in infected cells that sediment at 12–20s and have the same base composition as similar fractions found in non-infected cells that have been treated with actinomycin. 3. In the presence of guanidine, which completely inhibits viral RNA synthesis, these fractions are labelled to a greater extent than in non-infected cells.

The effect of cortisol on glycogen and fructose-1, 6-bisphosphatase in baby hamster kidney cells infected with Chlamydia trachomatis

1980 ◽  
Vol 26 (2) ◽  
pp. 135-140 ◽  
Author(s):  
Stella I. Reed ◽  
William D. Hann
Keyword(s):  
Chlamydia Trachomatis ◽  
Host Cell ◽  
Glycogen Synthesis ◽  
Kidney Cells ◽  
Baby Hamster Kidney ◽  
Bhk Cells ◽  
Intracellular Environment ◽  
Infected Cells ◽  
Baby Hamster Kidney Cells ◽  
In Cells

This study was designed to assay changes in glycogen synthesis which may occur as a result of cortisol treatment of chlamydial-infected cells. Monolayers of baby hamster kidney (BHK) cells, unlabeled and prelabeled with [6-14C]glucose, were treated with various concentrations of cortisol before (pretreated) or during (post-treated) infection with Chlamydia trachomatis. At designated times after absorption, the cells were harvested and assayed for total glycogen and 14C accumulation in glycogen. The total amount of glycogen accumulated in cells during the period of greatest chlamydial glycogen synthesis (36 h) was not affected by cortisol treatment. Cortisol treatment appeared to have retarded the accumulation of glycogen in treated infected cells until 30 h after infection. Treated infected cells prelabeled with [6-14C]glucose accumulated a greater amount of 14C in glycogen than untreated infected cells. All cortisol-treated, infected cells exhibited elevated levels of fructose-1, 6-bisphosphatase activity, whereas untreated infected cells did not. The hypothesis that cortisol affects chlamydia multiplication by altering the intracellular environment of the host cell is compatible with the results obtained.

Turbomolecular Pumped Electron Microscopy of Rubella Virus (In BHK Celis)

1968 ◽  
Vol 26 ◽  
pp. 204-205
Author(s):  
A. B. Taylor ◽  
G. C. Cole ◽  
M. A. Holcomb ◽  
C. A. Baechler
Keyword(s):  
Electron Microscopy ◽  
Rubella Virus ◽  
Phosphate Buffer ◽  
Fetal Calf Serum ◽  
Calf Serum ◽  
Basal Medium ◽  
Kidney Cells ◽  
Baby Hamster Kidney ◽  
Input Multiplicity ◽  
Baby Hamster Kidney Cells

An aliquot from a continuous fermenter culture of baby hamster kidney cells (BHK-21 Clone PD-4) (Wistar) maintained in Ca free Eagle's Basal Medium containing 2% Kaolin adsorbed fetal calf serum was planted in spinner flasks at 300,000 cells per ml, total volume 600 ml. After equilibration for one day at 35°C to insure that cells were in log phase, the culture was infected with the M-33-AGMK25 BHK-219 strain of rubella at an input multiplicity of about 6 TCID50 per cell. The virus was identified with specific rubella antiserum.Preliminary experiments had shown that such cultures would reach a peak or plateau HA titer of approximately 1:64, 24 hrs after inoculation and would continue to yield virus for 6 to 12 days. One hundred ml aliquot harvests were withdrawn daily and the culture was returned to volume with growth medium and incubation continued. The harvested cells were spun down rapidly at 2500 rpm per 15 mins., fixed in 3.7% gluteraldehyde in Ca free phosphate buffer saline, and post fixed in osmium tetraoxide. After dehydration, the cells were embedded in Epon 812 and cured approximately 20 hrs at 60°C.

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