Spontaneous Production of Type C Virus Particles in a Culture Derived from Rat Embryo Cells

Author(s):  
Elizabeth S. Priori ◽  
T. Shigematsu ◽  
B. Myers ◽  
L. Dmochowski

Spontaneous release of type C virus particles in long-term cultures of mouse embryo cells as well as induction of similar particles in mouse embryo cell cultures with IUDR or BUDR have been reported. The presence of type C virus particles in cultures of normal rat embryos has not been reported.NB-1, a culture derived from embryos of a New Zealand Black (NB) rat (rats obtained from Mr. Samuel M. Poiley, N.C.I., Bethesda, Md.) and grown in McCoy's 5A medium supplemented with 20% fetal calf serum was passaged weekly. Extracellular virus particles similar to murine leukemia particles appeared in the 22nd subculture. General appearance of cells in passage 23 is shown in Fig. 1. Two budding figures and one immature type C virus particle may be seen in Fig. 2. The virus particles and budding were present in all further passages examined (currently passage 39). Various stages of budding are shown in Figs. 3a,b,c,d. Appearance of a mature virus particle is shown in Fig. 4.

1982 ◽  
Vol 95 (3) ◽  
pp. 697-703 ◽  
Author(s):  
D H Carney ◽  
J S Bergmann

We used electron microscope autoradiography (EMAR) to visualize the interaction of 125I-thrombin with its surface receptors on mouse embryo (ME) cells. Autoradiographic grains were spaced over the surface of cells in a periodic nonrandom pattern, indicating 125I-thrombin association with clusters of thrombin receptors. The grain spacing varied slightly from cell to cell, indicating subpopulations of cells with different numbers of thrombin receptors. The average distance between grains on ME cells after binding 125I-thrombin (125 ng/ml) at 37 degrees C was 1.65 +/- 0.49 microns. The average distance between grains on prefixed cells and cells incubated with 125I-thrombin at 4 degrees C was not significantly different from that observed at 37 degrees C. This indicates that thrombin receptors are clustered before thrombin binding and that the thrombin receptor aggregates do not redistribute into large aggregates on the surface of cells subsequent to thrombin binding. The number of grains per cluster also does not change under these three binding conditions. Thus, the number of occupied receptors in each cluster appears to be constant. On the basis of the average grain number and spacing, we estimate that each cluster is approximately 400 nm in diameter containing approximately 550 thrombin-binding sites. These receptor-clusters are not associated with specialized structures or coated regions of the membrane. Additionally, grains observed within cells were not found associated with coated vesicles. Therefore, neither the clustering patterns nor internalization of 125I-thrombin are characteristic of molecules which bind to receptors and are internalized by receptor-mediated endocytosis.


1963 ◽  
Vol 17 supl. ◽  
pp. 55-58
Author(s):  
B. Skarzynski ◽  
M. Guminska ◽  
Z. Porwit-Bóbr ◽  
J. N. Baptist

Author(s):  
R. A. Al-Adhami ◽  
A. L. Chapman

Fujinaga et al reported MSV induced rat and hamster osteosarcoma which showed an occassional unusual bud in the rat induced tumors. Savage and Hackett and Hackett and Sylvester reported abnormal type C virus in UCLB cells derived from Balb/3t3 cells infected and transformed with MLV. They wer unable to demonstrate sarcoma virus activity. Fischinger and O‘Connor reported the infection of cat embryo cells by a centrifugally induced aggregate of murine sarcoma virus and feline leukemia virus designated as MSV(FelLV). This virus gave rise to a defective, focus forming virus which propagated in cat cells but not in mouse cells.In the present study the morphoiogy of the MSV(FelLV) virus obtained from Dr. Fischinger and maintained in our laboratory since 1970 will be reported. Feline embryo fibroblasts (established in our lab.) and Crandall feline kidney cells (Cutter-Haver-Lockhart, Shawnee, Kansas) were used in this study.


1970 ◽  
Vol 16 (4) ◽  
pp. 237-242 ◽  
Author(s):  
J. E. Bismanis

Administration of hydrocortisone to mice caused activation of latent nosematosis in at least 25% of the animals. The sporozoan parasite Nosema cuniculi could be demonstrated in the tissues of the internal organs and circulating blood by direct microscopic examination. Growth and multiplication of the parasite could be achieved in mouse embryo cell cultures, where the parasite infected and destroyed only about 2% of the cells, thus establishing a state of persistently infected cell culture. The parasite grown in cell culture retained its mouse pathogenicity.


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